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Radiation Effects Research Foundation
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A Japan-US Cooperative Research Organization
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A Brief Description
ZOE: A kg TLE INABA D BSE FT EI FEZ | RRR GE MI FEIT BME FEI
Front: RERF in Hijiyama Park, Hiroshima, Back: RERF Nagasaki Laboratory
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Radiation Effects Research Foundation
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A Brief Description
BX Contents
BX Contents
Bees SE! AIMMMOGUICHIONY: 24s eeseci resus At cedt acces a teens aa Panes Acta dacih ca ceeedes tniestteaeta etna a aac deae acess 1
BIL EBY E YAEE Objective and HIStory .o.cc.cccccccsccssessssssesseessessessssssecsscsssssscsucssscsscsusssecsucsussscsucsuecsecauessecscaseases 3
#8 FY Departments
PE=ZEB Department of Epidemiology ..........cssscssssssssocsrsessscscessssscssnsessessessaseassdnsessssvencaceusssseisaseosasnsassecsoasaseossoreese 4
HAL uy Department Of Statisties.seccasesveissdeacescussbaevasiesvascerndsvevinsovh acura tdasteseaiaeas des oenticeardienmies Gide 4
RAR SEER Department of Clinical Studies ......c..cccccscscsssssscseessssesecscssscsescsescsvssescscssescssscsussesescseeseseseseesesesesees 4
Gene ub:, Department OF Genetics v.ivsiséss.isieacscavehs cigesssexviahisasa aatsesnssestnsser a vivnentaacssaneacteen eataaasaueenaiensirn 5
NRE DW F/ a FEZ Department of Radiobiology/Molecular Epidemiology.........:.::cccssceseeseseeeeseseesees 5
THERELATES Information Technology Department .........ccscccccsscsessssesesessessscscescsesescsucscscssesessseaauescseseseseseseseseasess 5
BASSE Study Populations .........ccccccsscsscssssssccsessecssccsesssccsscssssscsucsaessccsssascsuccsssasssscsascssessssauecsssussauccsessscascssssaseeses 6
Frimiite (LSS) 42H] Life Span Study (LSS) Sample
De Me ech 2 (AHS) 486
hare Se] In Ute
MIRA OF TE (F,) OEE] Children of Survivors (F;) Sample ........cccccccscsscsessessescssssesseseesesscsessssesscsesssseeesseees 9
aur
=
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BUARO FHARZ2 Early Radiation Effects
FEVERU UIE Acute Radiation Syndrome ......ccscssssssssessessessessessessessessecsccsccscsscsscsessscsessessecsecscauccucsecseeseesesseeses 10
EMG (ce, AGUS IDG AUI ss2es cers 22s ccs davstorn shits tote ci Gea cacs earsecede stasecs sek oveea tomerate a eteaasn ea taaeaa feels ansdodtledeesh ateatese 11
OTR AABE CGA) Radiation Cataract (Lens Opacity) ..c..cecceccssessessessessessessessestestssteseeseeseeseeseeneenss 11
PETAR BRZE Late Radiation Effects o...ccccccccsecscssssssssssssessssecssnecssnecsssecsssecsssccsssccssecssssesuseessueesssceesneesseecsneesaes 13
BEI ACO Av. ISOlid Cancers «....icecsocasssovsse shasisescossasensxesseadvossedeneseeseg uevendcussedevsssivsnscdtssssnseaseaiensssvesvesseauaeveavesibtasisians 13
PUM pas. MSSM ec fas sas tresses cates tases ene eps cate eet ac atiesde san sseracc ga eanestoncs ceuens eas Ges sttens te eestees se eect scatters 17
TSE. “Benim MUmOrs yeasts saves, 5 vas d seveta rea scale devearsinc ce woes desist shaver te Ataacssisi ntearatete keane coed 19
PBAWNOREIC E SITE Non-cancer Disease Mortality
Bete Ee Chromosome Aberrations........cessssssscssssesssssessessesesscesssencevessssncvessescaensnssscsessezetsessessssscnseessnseasestaees
AH ZEAE SE ~— Somatic Cell Mutations ......c.cccccccsccsccecsececcesssceccscescsceeceevaceecsesscsessceecaccacsesseecsceacecsaceecaeeaceeeaces 25
Gegee ArMrivenity sess -2eseeeesscsecatiaaes aes seas es aigessav datas eased wei een dae erresaaieah i oee as 25
Wide + 38 Physical Growth and Development ...........::ccssssesessessssessesesseseseeseseeseseeuesecscsesaesessecesessseseesneneetenees 27
ZAG? JA SIND: Aiee acenaranensatihia tines hadtasatin dam emGinnalrniind dandinnaisiinkuatanaie: 27
HAA®ERE In Utero Exposure
ithe EOI ~=Mental Retardation and Growth Impairment ............c.ccesceseeseeseceeseeeeeeteeteeees 28
WS AISEEZE * Cancer Incidence iiss. wiainissainasiaaia terest ta uisatietamvenrainrinarntaraish cnet 28
PETAR OIBIRAV RZ = Geretic Effects oo... cccccccessessssessssessessssesessessssesessesseseesesessssessesesseseesesnesesssseeseseeseseesenesseanes 30
THAR REESE = Birth Defects in Fy OffSpring ........cccccccccsssscsessesescseseesesesessescscscsuescsescsuesescsesuesescscsesesssessescsceeeeees 30
ee Ls’ «Sex, Ratio mil Oftsprim % sccszaacdadecs tras cstedacsvasa oP eciveacecaca shaves tesecied acids tasdedensdul sched scalacedisbaastandanaeee testy 32
4e fa {KL Chromosome Aberrations in F, Offspring ....c..c.ceecccscssessesessssessesessesessesesecueseesesesseseesesnssesesseeneaeees 33
MRA AA DZ/KZES Blood Protein Mutations in Fy Offspring......c.cccccccccsesessessecseseseessesesseeseeseeseeseeseeneanes 33
DNA fae > DNA: Studies in: Fy Omtsprintgss.ctsicss.cesccsedgesnszceatcasesepsoenecassatanstcessartessseeancaonsban npeceiinttv aeessasseaeeasconaa 35
Contents BX |
FEC LOPS A584E 28 =~ Mortality and Cancer Incidence in Fy Offspring .......c..ccccescessessesseseeseeseeseeseeseeneenes 36
HEARS Radiation Dosimetry
PEREZ ASME REHE TE Physical Dose Estimates .........ccccsscscssssssssssessssesssscssssscsssvesssscsessssessssessesccussesessecseateseeecseeseaes 38
WRT SL — Residual Radiation ......ccccccccccccssscssesssscssescscescscesesscssescsscscssesesscsscsesacseacsecsesacssescsecsescasesssecstsacsecacsaes 40
FEA HE TE Biological Dosimetry .......c.cccccscssssesssssssssssesssscesssssssscssssessssesesnessssssecssacsisscsessecssaesescsesseaes 42
fs] .—7— _ Frequently Asked Questions
Mi dT a a aca daeen cesarean ae oc aed eedat om neaeaoeemnnnanA 44
Question 1. How many people died as a result of the atomic bombings?
BARES 2 FACES ARBRE UC REDS DSA FEE I esc eccceeccseeecseeecsneccsseessscecesecsesecsusecsnsessnseesssecsneecnseesuseesuseesaeeesntensesss 44
uestion 2. How many cancers in A-bomb survivors are attributable to radiation?
FR 3 WPA CE 2 ING PALES BEE CVD coccecceesesseeseeeseessneessneessneesseesseesniessaeesnies 45
Question 3. Are radiation-induced cancers still occurring?
Eel Aire a SO os cioniesdas cere aateeanctesiaisskescal eel conean Aan em Oae anaEsraniialn 46
Question 4. What radiation effects have been observed in people exposed in utero?
(214 2a sat pdt <n eee needa Cee emer ere eee orate cet eee a PCT CRTC ee Cee IT ree Teer ee ee me eee 46
uestion 5. What have been the genetic effects of radiation exposure?
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Question 6. Who make up the RERF study population?
Fi] i ae ed Se oe ey OAT) BUA seerdi wrens dcdcriecs tennraeen ecteibednd telecon wien maak einaaslaarlieen! 47
Question 7. What percentage of A-bomb survivors are included in RERF studies?
(A a Ue es eae a a ee on Bog |S | = gener nn eT ee 47
Question 8. What percentage of A-bomb survivors within the study populations have died?
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Question 9. What is meant by “significant dose” when referring to radiation exposure?
LTE) UO! YE eM SIS Hee a Oe Why D8 aca cendbnenbsaetavasesseapcacnsaanaasadbccadesinanasinaanaliye 48
Question 10. How long were Hiroshima and Nagasaki radioactive after the bombings?
HEAT OZFLL Collaborative Programs
HAEIAB LOR KM OEE Japan Domestic and Japan-US Collaborations .......cccccsseeseseeseeseeseeseeee 49
EARS HI & TEERSE18 ~~ International Collaborations and Information Dissemination..........c.ccscccccceseeseeeeeeeeees 49
Mah & ZOAFAR RERF Publications and How to Acquire THEM .....ccccccsesssesssesssesssesssessseeeees 51
HERD 5 OMMERFIAA Use of RERF Data by Outside Investigators ........ccccccccssesssesssesssesssecssecsseessecssecssecssecsses 51
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PLEZTAO AAICDUYT RERF Tours and Further Information ......c.ccccccccccsscssesssessesseessecseessesseesessecseessesseeseessees 57
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Introduction Fr3t |
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Introduction
The Radiation Effects Research Foundation (RERF) is
a research institute established in 1975 with joint funding
from the US and Japanese governments, as the successor
organization to the Atomic Bomb Casualty Commission
(ABCC), established in Hiroshima and Nagasaki by the
US National Academy of Sciences in 1947 to study health
effects among the atomic-bomb (A-bomb) survivors in the
two cities. RERF took over the long-term follow-up stud-
ies conducted by ABCC without making any significant
changes. Ever since that time, the institute has continued
its activities based on the mission of maintaining the health
and welfare of the A-bomb survivors and researching
radiation effects on human health under the unique joint-
management arrangement by the two governments.
ABCC-RERP'’s research aim is to determine long-term
effects of radiation exposure, which had been uncharted
territory for scientific research. More than 60 years have
already passed (as of 2008) since the initiation of the
follow-up studies, but nearly 40 more years will be needed
to complete follow-up of those who were young at the time
of exposure. Thus, it must be said that RERF’s research is
only half done. Despite that, however, quite a few findings
have been uncovered by past research, and the organiza-
tion’s research results have been utilized as reference in
medical care and welfare for A-bomb survivors, consis-
tently attracting the attention of international and other
organizations as a source of basic information for establish-
ing radiation protection standards.
RERF research is characterized by the long-term follow-
up of a large well-defined population. The scale, structure,
and accuracy of the follow-up studies are unparalleled any-
where in the world. Health examination participation rates
have remained high over many years. That RERF has
maintained such a high level of research is thanks to the
understanding and cooperation of the A-bomb survivors.
At the same time, RERF’s achievements would not have
been possible without cooperation from related local
organizations, for which we would like to express our
sincere appreciation.
Another strength of RERF research is that the radiation
dose of each A-bomb survivor has been estimated with a
high degree of accuracy. The first RERF radiation dosime-
try system was announced in 1965, followed by two revi-
sions, in 1986 (DS86) and 2002 (DS02). Starting with this
version of our brochure, we are now using doses estimated
with the DSO2 system. Doses estimated based on the DS86
system will continue to be used for referring to research
results obtained during the DS86 period, and doses esti-
mated based on the T65D system will be used in the same
way. The main differences between DS86 and DSO2 are
the accuracy of the data used and the methods of calcula-
tion; the basic philosophies and the dosimetry systems
real FX Introduction
ED FNS RO & Bi LT. PEP 10fF LES
DERY VRE CERT SY—AVE (Sv) CHUTE
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themselves do not significantly differ. Differences in indi-
vidual doses estimated with the two systems are numerous,
but on average, DSO2 doses are higher than DS86 by about
8%, and as a result, the risks of effects per unit dose are
slightly lower. Please refer to the comparison table below
for details.
Because of differences between the biological effec-
tiveness of gamma rays and neutrons, we have used
weighted doses—the sum of the gamma dose plus 10 times
the neutron dose. Formerly we designated this with a dose
unit called sievert (Sv). However, more recently, for this
same calculation, we have expressed the unit as “weighted
gray (Gy),” which will be employed in this brochure. One
reason for the change is that the Sv unit is mainly used for
radiation protection purposes rather than for risk estima-
tion. Another reason is that the International Commission
on Radiological Protection (ICRP) applies tissue weight-
ing factors in deriving Sv estimates; those tissue factors are
not applicable to the A-bomb exposures, so it causes confu-
sion to apply Sv units to RERF doses.
DS86 & DS02 OME t
Differences between DS86 and DS02
DS86
JA & Hiroshima
eet 17 Bomb yield
E38 aE Height
LE SASINE
15+U hy 15 kton
580 m
Ba 14. Location
WY viist Gamma-ray dose
Hp
Fist Neutron dose
fell} Nagasaki
eet HJ] Bomb yield
HRS Height
E3801 Location
2140} Y 21 kton
503 m
HE tse Neutron dose
DS02
16+ bY 16 kton
600 m
15 m Pi-\f%8) Moved to the west by 15 m
Ai FHI (1LO%LAA) Slight increase (<10%)
45 Fit Slight decrease
Zt 72 L No change
2% 72 L No change
3 m PU\*28) Moved to the west by 3 m
1-2km C#Fi8h (#4) 10%) Slight increase at 1-2
km (about 10%)
2-3 km CijitZ> Decrease at 2-3 km
1-2 km 6 25% L)_ EO iik“> Decrease by more than 25%
at 1-2 km
Objective and History KILO BN CIA ff
ILO AN CAS Objective and History
ax 2) BAY Objective
AAO Fic, BUND IUKIC RIES REN EB E The objective of RERF is to conduct research, for
UCHIZE SPIE AIELLO ERE MERE LU peaceful purposes, on the medical effects of radiation on
bic torevic, BAO ILE ICRA man, with a view to contributing to the health and welfare
fi FURS 4 I. AGO PME AAO TALE: (= 65 F- of the A-bomb survivors and to the enhancement of the
ALECHA HUCMANITA. 34%, 1975 4F). health of mankind (Act of Endowment, Article 3, 1975).
® = History
BUwls, ARBIRIRICHEOAR, AROS - BARA RERF was established on 1 April 1975 as a nonprofit
AWE L. #7: AKERS CEB ZB ASE foundation under Japanese civil law, within the jurisdic-
i A Ac3 joo Met _,, | tion of the Japanese Ministries of Foreign Affairs and
MELT INS F4 HV AIREL A BIE 1947 SICK Health and Welfare, and in accordance with an agreement
pa
ESD BAAO Bal Lo CABREL BEA LE | between the governments of Japan and the United States.
ABCC CH). 224A ICID B EDLY EER ASAI =| «~RERF was preceded by ABCC, which was established in
LC, SECA 2: HEIRS © REFURB Lee. 1955 1947 by the US National Academy of Sciences with fund-
KILI G vy ABBA L ZAHEER GDN. % ing from a US Atomic Energy Comnussion. mpee initi-
ated extensive health studies on A-bomb survivors in coop-
van Aa =. a)- A Zr Beaad ay é am : :
Om, WRATH A URS SUI SUT A 8 IT BLT eration with the Japanese National Institute of Health of
AAO TEPER SE DIE 0 the Ministry of Health and Welfare, which joined the
1975 42.0 Hi SZtA@ Pea RIC. «HOKE IC £ aR research program in 1948. A comprehensive review of
Hee DEM ZLERON. CHEE. fit ABCC work in 1955 (the Francis Committee) led to exten-
we ee os poet a sive revisions in research design and laid the foundation
SATO AEE BRS ROBES Lo CHS SHEA | for the population-based studies that continue today.
(TV, wa ROT SE a BS EO BE CHR S 114 BP When ABCC was reorganized to form RERF in 1975,
ame AR OE UTS Fe CED ON TWD. HEE k
REHOME L. WEILA ARISE SHS SIR. ORE nership between Japan and the United States. Accordingly,
REREF is managed by a binational board of directors, and
its scientific research activities are guided by the annual
sy
jij | it was deemed essential that research continue in full part-
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recommendations of a binational scientific council. Funds
for RERF’s operation are provided by both governments,
by Japan through the Ministry of Health, Labour and Wel-
fare, and by the United States through the Department of
Energy.
0) S8F5 Departments
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Departments
Department of Epidemiology
The primary task of the Department of Epidemiology
is to clarify through population-based studies the risks
associated with human radiation exposure. For almost 50
years, follow-up studies of more than 200,000 survivors
and their children have been conducted through the Life
Span Study (LSS) cohort of A-bomb survivors, the cohort
who were in utero at the time of the bomb, and the F,
cohort of persons conceived after the bombings. Analyses
focus on mortality and cancer incidence in relation to radia-
tion dose, allowing for risk factors other than radiation.
The LSS is the most important epidemiological study of
radiation effects in humans in the world both because of
the size and well-characterized nature of the study popula-
tion and because of the duration and completeness of
follow-up studies.
The department is also entrusted by Hiroshima city,
Hiroshima prefecture, and Nagasaki prefecture to operate
local tumor registries. The collected data serve as a unique
source of information on cancer incidence for both A-
bomb survivors and the general population.
Department of Statistics
The Department of Statistics analyzes the information
collected by other departments on radiation effects, pro-
vides statistical support and advice to research scientists in
other RERF departments, and assists with data manage-
ment. Members of the department aid in designing studies,
and they develop and apply statistical procedures for ana-
lyzing RERF’s unique research data. Management of the
dose information and calculation of individual doses are
further responsibilities of the department.
Department of Clinical Studies
The Department of Clinical Studies conducts biennial
medical examinations of participants in the Adult Health
Study (AHS), a selected subset of the LSS and in utero
cohorts. The AHS program was begun in 1958. In addition
to standardized clinical examinations and routine labora-
tory tests of blood and urine, special tests are conducted,
for example, to detect bone density changes in postmeno-
pausal women, perimenopausal hormonal changes, cogni-
tive impairment in the elderly, and various other disease
conditions, such as cataracts, thyroid nodules, and uterine
tumors. Biochemical and physiological data from these
examinations enable long-term evaluation of the health of
A-bomb survivors. Participants are fully informed of
examination results and, if necessary, are referred to local
physicians for further evaluation and treatment. Accumu-
lated data are used in epidemiological and clinical studies,
and biological specimens are stored for use in laboratory
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research on radiation health effects. The AHS is one of the
most comprehensive clinical follow-up studies ever under-
taken. Although examinations are voluntary, participation
rates are regularly between 70 and 80%.
Department of Genetics
The Department of Genetics performs cytogenetic and
molecular genetic studies. In the cytogenetics laboratory,
long-term research on the frequency of chromosome aber-
rations in lymphocytes from A-bomb survivors is carried
out to aid in assessing individual radiation doses. The labo-
ratory also uses the electron spin resonance method to
evaluate radiation doses recorded in tooth enamel. In the
molecular genetics laboratory, studies at the DNA level
use blood specimens provided by survivors and their chil-
dren to determine if mutation frequencies in offspring are
related to parental radiation dose.
Department of Radiobiology/Molecular
Epidemiology
The Department of Radiobiology/Molecular Epidemi-
ology comprises the cell biology and immunology labora-
tories, which investigate somatic mutation frequencies in
blood cells, mutations of oncogenes and tumor suppressor
genes in cancer tissues, and possible radiation effects on
immune function. Tumor specimens stored over several
decades, mainly by local pathologists in Hiroshima and
Nagasaki, are analyzed with newly developed molecular
biological techniques.
Information Technology Department
The Information Technology Department comprises
the Systems Technology Section and the Library and
Archives Section.
The Systems Technology Section provides, maintains
and integrates RERF computers, maintains the RERF net-
work under secure conditions, and develops various data-
bases and application programs necessary for RERF
researchers. Further, the section is also involved in techno-
logical cooperation with organizations both inside and out-
side of Japan.
The Library and Archives Section supervises RERF’s
professional library, with its focus on radiation medicine
and biology, and carries out work related to the publication
of RERF research papers in scientific journals. The section
collects, stores, catalogs and manages research papers, aca-
demic meeting presentations and other important ABCC-
RERF materials, making available such information on
RERF’s Internet homepage. It also responds to inquiries
from both inside and outside RERF and to requests for
papers and documents.
§) AE Study Populations
il Se
1955 4EI2 ABCC IL, VI YYARRRSOMEELZLUIT,
1950 46D EAA ASE CFT 0 11 7o RRS ED 5 435 1
RANEY CT. AERMOM RG Ie NES A OB
Wie Ais fem Le. CORAM AIC LY 2854-108
AS) BEE DERE S TL. COP OR 20 7B ADS 1950 4 4 HE
BES: RRO SAA IMEL Cuz (SEATS). 1950 4E
BAL LIME, ABCC — BURT CSI S eR AE IS
TATOO [HAH] POBIINLAMKEM ICO CHD
MeKR (H1)o MURMACL, FRAGA - EBEO
ASEH eC. FIA Ca ABR Y ILE L 7 HK IC Ado
0 te < TORIC Ste ALLIS. BAD BABS
BEL Clk, WIMO MEG + ACRE b OTR OA mol, J
IFUL (CPR SIS) (CLO MAE TOTS. AMS BIE
Yam
Study Populations
In response to the recommendations of the 1955 Francis
Committee, ABCC used data from the A-bomb survivors
survey, conducted at the time of the 1950 Japanese national
census, to develop a comprehensive roster of persons eli-
gible for inclusion in fixed study cohorts. The survey iden-
tified 284,000 Japanese survivors, of whom nearly 200,000
were resident in either city at the time of the census.
Subsamples of this original Master Sample have formed
the basis for all studies conducted by ABCC-RERF since
the late 1950s (Table 1). In all mortality studies, informa-
tion on cause of death, regardless of location in Japan, is
obtained through official permission from the Ministry of
Health, Labour and Welfare and the Ministry of Justice.
Information on cancer incidence is obtained through the
local tumor and tissue registries and is limited to current
residents of Hiroshima and Nagasaki prefectures. Addi-
(OV Clk, KB OSE & EREIRBE ICES 4 IBHINFER DS & | tional information on disease incidence and health status is
Ze available for AHS participants.
#1. ERMA TUF IA EHRAR
Table 1. Major RERF research programs and population sizes
a) AE AT AE
Studies Subjects
Firat: Life Span Study 120,000
py eked te Adult Health Study 23,000
IRAE Hz = In Utero Study 3,600
i {ta*f Ze ~=Genetic Studies
TK EASA EZ ~=Mortality and Cancer Incidence 77,000
Mitta 4 ~=Cytogenetic Studies 16,000
ifa(ta# Biochemical Genetic Studies 24,000
43 F-iateedd4e Molecular Genetic Studies 1,500
fii As EE we #E «= Clinical Health Survey 12,000
Fimadz (LSS) Hi Life Span Study (LSS) Sample
“40 LSS EAL. [ZEAE CE EN SREAOHTC,
AR CAR OMTTEML) DRED CH. 1950 ECT
DERSMICFELEL. BRN HEB AE & WY REIS TS EHD
\lRUT 6 AUT RHE eM ET AOD 5S THIOL DP
(CUANZA DPOSHMANTWS,. FRbdDb, BLO
sLth2> 5 2,000 m LIA CHER L 7 [SEAT | PER aE a5
BAHU TV-G EEREREET) . 58 2 TR: BRD 2 5
2,000 — 2,500 m C#REE L 72 [ARATE] SRS TR: 1
PEL EWG TERS -BRTSD EDEN BEDI 5S 2,500-
10,000 m CHER LZA GH IRRERURE). BLOG 4 TF:
As initially defined, the LSS cohort consisted of a sam-
ple of survivors from the Master Sample who were resid-
ing in the cities in 1950, whose honseki (place of perma-
nent family registration) was in Hiroshima or Nagasaki,
and who met certain eligibility criteria that would facilitate
effective follow-up. The LSS originally included a) a core
group of all eligible Master Sample survivors who were
within 2,000 meters of either hypocenter at the time of
bombing (ATB) (proximally exposed); b) all eligible
persons in the Master Sample within 2,000 and 2,500
meters; c) a sample of eligible survivors between 2,500
and 10,000 meters (distally exposed), matched to the a)
Pek
as
1 EG EDS Be HLF CHIEN 7, 1950 SET
*AICIK ES + RIC TERE LC 2 PSUR IST AIC
POKACH So 54 HIDE AATES CMPD, J
RR S0OHUADAT SH CtnUMOATHb BENTH
Bo
2447) 99,393 Ade 5 fink S Cvs LSS BAIS. 1960 4246
BRAFICHEK SN, ABM IC BER ¢ 2,500 m DLA CHEER L
te [SEAHE| @R BOK. UVC 1985 iC MICU KS tr
C [AH] OS RIFRREAS EO 5h, FA CIRO
ASULG FF 120,321 Kt BoTWS ($H2). COBB,
ke Litizs 6 10,000 m LAA CHER L 7 93,741 A & JEUERIRFTHA
AER 26,580 ABE EN THA CNS 93,741 ADF 5,
86,671 AlZOvs Cla PRR ae HE FE OT 5 TL TWD DS,
7,070 A (2 D4 b 95% tk 2,500 m LIA CHEEL TWH) UZ
OV TILE? HUFB IC LB WERT D BEHE S PARTS Ze UE
KP FOR OM MAHL CA TRV. BIE. LSS EE
Study Populations H&E fj
group by sex and age; and d) a sample of persons, age- and
sex-matched to the a) group, who were living in Hiroshima
or Nagasaki in the early 1950s but who were not in either
city ATB. The so-called “not-in-city” group included peo-
ple who entered Hiroshima or Nagasaki within 30 days of
the bombings and others who returned to the cities at later
dates.
The original LSS cohort included 99,393 persons. In
the late 1960s it was expanded to include all Master Sam-
ple survivors exposed within 2,500 meters regardless of
place of family registration. In 1985 the cohort was further
expanded to include all Nagasaki survivors in the Master
Sample. At present, the LSS cohort has 120,321 members
(Table 2), including 93,741 survivors who were within
10,000 meters of the hypocenters and 26,580 persons not
in the cities ATB. Among the 93,741 LSS survivors, indi-
vidual dose estimates are available for 86,671. Because of
complex shielding by buildings or terrain or inadequate
shielding data, doses cannot be evaluated for the remaining
7,070 survivors, 95% of whom were exposed within 2,500
22. AiMmMELMOARE HERAT (DS02)
Table 2. LSS subjects by estimated radiation dose (DS02)
LSS 42HIO AB
LSS subjects
BANU Leekiiiie (Gy) Wy is Fe IG & at
Weighted colon dose (Gy) Hiroshima Nagasaki Total
<0.005 PAINS} 16,823 38,536
0.005—0.05 17,207 6,227 23,434
0.05-0.1 5,507 1,005 6,542
0.1-0.25 6,273 1,270 1,048
0.25-0.5 3,842 956 4,798
0.5-1.0 2,376 1,052 3,428
1.0-2.0 1,151 614 1,765
>2.0 436 189 625
Be # a Ni)
CER ENA 3,449 3,621 7,070
Dose unknown
Bae AS
Bua Ar 61,984 31,757 93,741
Total survivors
AA ES (LAT)
Not in city (early entrants) pyiee oat eet
HAA eA)
Not in city (late entrants) 16,238 8,823 aU 26t
Se De
ies ant 20,230 6,350 26,580
Total not in city
: Ae
LSS RE Set 82,214 38,107 120,321
LSS total
§) AE Study Populations
(cla, TAEAREE] (ICA TW 2,500 m WA OPED UE
SABENSDS, Rica 4 ia LBA NTs
So. FRbb, 1950 4 AEE CIHR L RR E (1950
EAR AO HAO 30%). HARIZEIC MAO BR
FURIE HTC O A ARERR, BL OSE
Fe (CHELA, HEARS) deen TRY, WEOTE
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LOGREAFCE 4S. 1958 FORA, AHS 524
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PERL. AERC UIE © AR LL 72 4,993 ASA RSMS. ©
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3,500 m, fellfi-Clt 3,000 — 4,000 m OPFARE CHIR LEA, B
EU 3) URC STHOMC SAPO ATCHS.
1977 F<, eR BUR OWL & REL TC. MAKI SO
O77 V—-Fx lz AHS BAM LUKL, Fat 23,418 LE LZ.
tb, 1) LSS#HOI 5, 1965 EEE RN LDS
1 Gy LE CHS 2,436 \OWIRAEA, 2) CNS6OK EF
Hinds LOE ECS AZ ARO IR, BLOB) HR
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2005 *ESIZE. 1 AGE < DATEL TAD, FOI 5H 6
FA ASAT MIRAE LY BIS SD 70% (BLE
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AUSRICZEOR. JAAR O [MPR AAL) BO [FECES
EAE | OR OIL LODO BET J AERM PRE S 1,
AIA AS PARA S AL 0
meters. While the LSS now includes virtually all survivors
from the Master Sample who were within 2,500 meters of
the hypocenters ATB, there are other proximal survivors
who are not included. In addition to survivors who had
moved away from the cities by the late 1950s (about 30%
of the 1950 census survey respondents), the LSS does not
include survivors who did not respond to the survey, Japa-
nese military personnel stationed in the cities ATB, and
non-Japanese citizens (e.g., Chinese and Koreans). It is
believed that the cohort includes about half of all survivors
who were within 2,500 meters of the hypocenters ATB.
Adult Health Study (AHS) Sample
The AHS was created to collect disease incidence and
health information through biennial medical examinations
of LSS survivors. The examinations make it possible to
diagnose the full spectrum of human illnesses and physiol-
ogic disorders, to study incidence patterns for both cancers
and non-cancer diseases in relation to radiation dose, and
to obtain clinical and epidemiological information not
accessible through the records-based mortality and cancer
incidence follow-up of the full LSS cohort. When estab-
lished in 1958, it consisted of 19,961 persons drawn from
the original LSS. At its core were all 4,993 survivors
known to be alive in 1950 who were within 2,000 meters
of the hypocenters ATB and who reported signs and symp-
toms of acute radiation syndrome. The remainder of the
AHS included three city-, age-, and sex-matched samples
drawn from the LSS, each similar in size to the core group.
The three groups were: a) survivors without acute radiation
syndrome who were within 2,000 meters of the hypocen-
ters ATB; b) survivors 3,000 to 3,500 meters from the
hypocenter in Hiroshima and 3,000 to 4,000 meters in
Nagasaki; and c) persons not in the cities ATB.
In 1977, because of concerns about attrition among
high-dose survivors, the original AHS sample was
enlarged to 23,418 persons by adding a) all 2,436 surviv-
ing LSS members with assigned tentative 1965 dose esti-
mates in excess of one gray, b) an equal number of age-
and sex-matched distal controls, and c) 1,021 in utero-
exposed survivors. As of 2005, nearly 50 years since the
creation of the AHS cohort, nearly 10,000 cohort members
are still alive, of whom about 6,000 live in the contacting
areas and 70% of them (nearly 4,300 members) continue
to participate in the AHS clinical examination programs.
In Utero Sample
Various studies of persons exposed in utero were cat-
ried out during the 1940s and 1950s. Beginning in 1960,
two overlapping fixed cohorts, one for clinical studies and
one for mortality follow-up, were assembled from records
of about 10,000 births occurring in or near Hiroshima and
Nagasaki between the time of the bombings and the end of
May 1946.
[RACE ARSE | Uk. ee
LKEA@EBE,
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WHE Bt. 1,608 AAO O
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AIZBIL Tl 0.005 Gy DI
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(1118 A) POMARDAV-Pk, bie c
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(\CEBS SAA Cla, RRP ARSEAT & FETS RSE
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20 TBY. F044 1,060
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BUN Ra Os
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ABCC ICBIFS MMO CL, BIRO LENO ifs
WED SS SLICE S24 CHK. 1950 EAABIZE Clic,
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(LOU CHIARA TT DILTEDS, RAHA O SLES BS
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Lko COPEICBOS. F, FECA AE AAS 1950 4EACIC
OUNCE SN, TOPRZ RI DK YUKSNK.
“OO F, SAIL, 1946425 A 1 AAS 1958 4F RE Cle
AEE ALTE 54,243 AP5 BY. CO 5D 53,518 Al2OwT
EET — FAME SNCS. HAW Tld, PRC ES
POA BLA 5 2,000 m LIA CHEER L Fe F HE
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WS 10,000 m WAI RABoORADEILN. SOROUL
KOA, F, MIS 88,485 Al AR. TRbob, HHO
bie < & &-HAGEK LSS BMI FEN, 1946465 8 1 7
PS 19844F 12H 31 AOMICEENKT NCO LHI
brik. KRRLIELMREMILW 7A TTACH A. OO
F, MOBO AUCH L CHAN A, EE El
ete CREA Ze ABCC — RUSH AA AEIE TTF DAFT DIL
CAs
Study Populations B#H fj
The clinical cohort included all Japanese survivors in
utero within 1,500 meters of the hypocenters ATB,
together with sex- and city-matched samples of similar
size from two comparison groups. This cohort includes
1,608 persons, of whom a subset of 1,021 were enlisted as
voluntary participants in the AHS.
The mortality cohort includes 2,817 subjects, 771 of
whom are also in the clinical cohort. The mortality cohort
was established in 1964 and consists of all persons
exposed in utero within 2,000 meters of the hypocenters
(1,118 survivors) with matched comparison groups.
Current analyses of mortality and cancer incidence
among persons exposed in utero make use of combined
data from these two cohorts. This combined group now
includes 3,654 persons of whom 1,060 have estimated
doses of 0.005 Gy or more (mean dose 0.28 Gy).
Children of Survivors (F,) Sample
The search for evidence of detectable genetic effects in
the children of survivors was a primary focus of early
ABCC research. By the early 1950s, based on data on birth
defects and early deaths in about 77,000 births, it appeared
that data on early signs of genetic effects provided no evi-
dence suggesting any dramatic effects. Nevertheless, the
Francis Committee in 1955 recognized the need for contin-
ued follow-up of survivors’ children and suggested that a
fixed cohort be defined. On the basis of that recommenda-
tion, the original F, mortality cohort was defined in the
1950s. It was later enlarged on three occasions.
The original cohort included 54,243 persons born
between | May 1946 and the end of 1958; follow-up data
are available for 53,518. The cohort included a) all eligible
children with at least one parent within 2,000 meters of
either hypocenter ATB and b) two sex- and age-matched
comparison groups of the same size as the core. The first
comparison group included children with at least one par-
ent exposed between 2,500 and 10,000 meters. The second
group included children with neither parent within 10,000
meters. Later extensions increased the F; cohort size to
88,485 by adding all children born between 1 May 1946
and 31 December 1984 with at least one parent in the
extended LSS cohort, but the epidemiological study cohort
consists of about 77,000 children. Overlapping subsets of
the F, cohorts have been used in various ABCC-RERF
study programs, including cytogenetic and biochemical
genetic studies.
Wh HO FBS Early Radiation Effects
WHR BSS
SER hee
PERCE] CMP ASN SRABIL, HO BUR
(J 1-2 Gy 5 10 Gy) (CER L RD 5 BH AOC
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Early Radiation Effects
Acute Radiation Syndrome’?
Illnesses collectively called “acute radiation syn-
drome” occur within a few hours to months after exposure
to high-dose radiation (from approximately 1-2 Gy to 10
Gy). The principal signs and symptoms include vomiting
within a few hours, followed within days to weeks by
diarrhea, reduced blood cell counts, bleeding, hair loss
(epilation), and temporary male sterility. Diarrhea results
from damage to cells lining the intestines, reduction in
blood cells from death of hematopoietic stem cells in bone
marrow, and bleeding from declining blood platelets gener-
ated from such stem cells. Hair is lost due to damage to
hair-root cells. Hairs do not fall out but rather become thin-
ner and eventually break off. Sterility occurs in men from
damage to sperm-generating stem cells.
Except for vomiting, these signs and symptoms are
closely related to frequency of cell division, rapid cell divi-
sion being more sensitive to radiation than slow division
(e.g., muscle and nerve cells). If the radiation dose is low,
the syndrome will seldom if ever occur. Conversely, if the
dose is high, death can occur within 10 to 20 days after
exposure due to severe intestinal damage, or subsequently
within one or two months, mostly from bone marrow
failure.
Figure | shows the relation of severe epilation (loss of
more than 2/3 of scalp hair) to radiation dose. Although
there is only a small effect up to | Gy, epilation increases
sharply with dose thereafter. (Above 5 Gy, the declining
frequency probably reflects overestimation of dose.)
Ba 1. BEDE & BR RR BE RIE ?
Figure 1. Severe epilation and radiation dose”
100
80
fo>)
(=)
BEREDZE (%)
&
Percent with severe epilation
20
0 1.0 2.0
HY VRE PEFIROS
3.0 4.0 5.0 6.0
atte (Gy)
Total dose of gamma rays and neutrons (Gy)
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Early Radiation Effects HAGOFHES fj
Acute Death‘
The probability of dying directly from radiation expo-
sure depends on the dose received. A commonly used
index is the dose at which 50% of a population dies (LDso
= 50% lethal dose). Acute death is defined as death within
about two months of exposure. At the LDs, level, bleeding
and infection due to immunodeficiency resulting from
bone marrow depletion are the main causes of death.
Recovery from such depletion sufficient to prevent death
usually occurs within two months.
Early estimates from survivor interviews measured the
LD, in terms of the distance from the hypocenter at which
50% of people survived: 1,000 to 1,200 meters in Hiroshima
and 1,000 to 1,300 meters in Nagasaki. Dose estimation
was not possible at that time because of insufficient shield-
ing information. Later analyses of extensive records at
RERF were able to make estimates of shielding and to cal-
culate that a bone marrow dose of 2.7 to 3.1 Gy caused
50% mortality within 60 days (with the new DSO2 dosime-
try system, the corresponding doses would be 2.9 to 3.3
Gy). The data came from about 7,600 survivors in 2,500
households exposed inside Japanese houses located within
1,600 meters of the hypocenter in Hiroshima. Survivors
inside Japanese houses received special scrutiny because
the homogeneity of such housing structures allowed better
estimation of individual radiation doses. The closer one
was to the hypocenter, however, the higher the radiation
dose received and the more severe the effects of blast and
heat in terms of destruction of houses and subsequent fires.
It was thus impossible to classify deaths that occurred
within a few weeks after the bombings as due to radiation,
injuries, or burns. To avoid deaths from injuries and burns,
the above RERF analyses therefore focused mainly on
delayed deaths; such deaths peaked at about one month
after exposure.
Based on this information from A-bomb survivors,
together with other information from cases involving expo-
sure to accidental radiation or radiation therapy, the United
Nations’ Scientific Committee on the Effects of Atomic
Radiation has estimated the bone marrow LDsojo at
around 2.5 Gy when little or no medical assistance is avail-
able and at 5 Gy or more with extensive medical care.
Radiation Cataract (Lens Opacity)*®
Radiation cataract causes partial opacity or cloudiness
in the crystalline lens and results from damaged cells
covering the posterior surface of the lens. Symptoms can
appear as early as one or two years following high-dose
exposure and many years after exposure to lower doses. It
is unclear how frequently radiation cataracts advance to
severe visual impairment, although we have documented
in a recent study about a 20-30% excess at | Gy of cata-
racts that prompted cataract surgery. A low-dose threshold
may exist below which radiation cataract does not arise,
&HRO PMB Early Radiation Effects
OEE Ce Mkt CO [LAV] BHSDbLNE
DWEBLSNTOOD, MILO MAC. LAVMHILAY
PD HokeELTSH 0-08 Gy HE CLRV DE RIBS
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although our recent analyses suggest that there may not be
a threshold, or if one exists, it is somewhere in the range of
0 to 0.8 Gy. The excess cataracts seen are of the types gen-
erally associated with radiation: posterior subcapsular and
cortical cataracts. Figure 2 shows the relation between
radiation dose and cortical opacity of lens.
Bel 2. AH PRB TDG BRL BURL ©
Figure 2. Cortical opacity of lens and radiation dose®
Ay ZX be
Odds ratio
OR/Sv = 1.29 (95%CI: 1.12, 1.49)
2 4
BAHIITLEARRS (Gy)
Weighted eye dose (Gy)
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BAH: RIFMBTOR MAI LY RItonk.
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JEG EERMLIA ES Clk 1957 46, Ril Clk 1958 4E (CBA S
ire. 195846225 1998 4EOIH IZ, LSS SMO CHEE
2 0.005 Gy LLE® 44,635 AHL 7,851 Alc Alig IO 28
Ay (TI AIC ERORA EE CRGEIL, KMD LODOA)
PRWESN, TRVEPIIE 848 Hl (10.7%) EHEERNTY
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Late Radiation Effects KHGORZS fl
Late Radiation Effects
Early radiation effects, such as acute radiation syn-
drome, result from doses high enough to kill cells and thus
cause direct tissue damage (1 Gy or greater). In contrast,
late effects, such as cancer (and possibly other diseases),
reflect DNA mutations induced in living cells by radiation
exposure. While the exact mechanisms by which such
mutations lead to cancer are not clear, it is believed that
the process requires a series of mutations, accumulated
over periods of years. Mutations can occur either spontane-
ously or as a result of exposure to any of a wide range of
environmental mutagens, including radiation. Since many
years must pass before a given cell and its progeny acquire
sufficient mutations to result in clinical disease, excess
cancers attributable to radiation do not become evident
until years after exposure (or somewhat fewer years in the
case of leukemia). Excess cancer risks in RERF data
correspond broadly with the age-time patterns predicted by
such hypothetical considerations.
Solid Cancers
Increased risk of cancer is the most important late
effect of radiation exposure seen in A-bomb survivors. For
cancers other than leukemia (solid cancers), excess risk
associated with radiation started to appear about ten years
after exposure. This was first noted by a Japanese physici-
an, Gensaku Obo, in 1956, and it led to continuing compre-
hensive analyses of cancer mortality and to the creation of
tumor registries by the city medical associations in both
Hiroshima and Nagasaki.
For most solid cancers, acute radiation exposure at any
age increases one’s cancer risk for the rest of life. As survi-
vors have aged, radiation-associated excess rates of solid
cancer have increased as well as the background rates. For
the average radiation exposure of survivors within 2,500
meters (about 0.2 Gy), the increase is about 10% above
normal age-specific rates. For a dose of 1.0 Gy, the corre-
sponding cancer excess is about 50% (relative risk = 1.5).
Tumor registries were initiated in 1957 in Hiroshima
and 1958 in Nagasaki. During the period from 1958 to
1998, 7,851 malignancies (first primary) were observed
among 44,635 LSS survivors with estimated doses of
>0.005 Gy. The excess number of solid cancers is esti-
mated as 848 (10.7%) (Table 3). The dose-response rela-
tionship appears to be linear, without any apparent thresh-
old below which effects may not occur (Figure 3).
Wh RHO BRS Late Radiation Effects
#3. LSS LMR SRIBAAREDY AZ (EH). 1958 - 1998 4 1°
Table 3. Excess risk of developing solid cancers in LSS, 1958-1998"
28A Cancers
BAC L oti aie ee en ee
Weighted colon dose WRAL PARE HET BL a 28
(Gy) LSS subjects Observed Estimated excess Attributable risk
0.005-0.1 27,789 4,406 81 1.8%
0.1-0.2 5,527 968 75 7.6%
0.2—0.5 5,935 1,144 gs) 15.7%
0.5-1.0 3,173 688 206 29.5%
1.0—2.0 1,647 460 196 44.2%
>2.0 564 185 111 61.0%
at Total 44,635 7,851 848 10.7%
3. LSS RMI BItS ABA A BE OBA XZ (BUR). 1958 — 1998 461° RU ERRIL, BERENE ERD 30 ig—D
AB 70 BITE LUA YG TL OR, BR FHI Y XZ (ERR) ORVERUEIUS SRF. KUDU,
PKA XZ EAE LIED YING RA BU YZ HEN CH ORO BEBE © OFFA CHEE EO
EF 1 RRERECRT.
Figure 3. LSS solid cancer incidence, excess relative risk by radiation dose, 1958-1998." The thick solid line is the
fitted linear sex-averaged excess relative risk (ERR) dose response at age 70 after exposure at age 30.
The thick dashed line is a non-parametric smoothed estimate of the dose category-specific risks and
the thin dashed lines are one standard error above and below this smoothed estimate.
RIS AZ
Excess relative risk
BAIT Litt e (Gy)
Weighted colon dose (Gy)
JERE BIC EO PERE NCASA SAU ATER GEDRI-AEVE The probability that an A-bomb survivor will have a
VAX) lt, SIPC SRMERSS LOVE HRA LC) Cancer caused by A-bomb radiation (excess lifetime risk)
7 ae cok depends on the dose received, age at exposure, and sex.
WA. M4 lc, 1 Gy (CRE LEO IY AZ & eB Fi ian
igure 4 represents excess relative risk and excess absolute
MEM VAD (HRP) ENF. CHSOMAY AZ 0, risk (sex-averaged) exposed to 1 Gy. Both expressions of
PUREMEIDYRUIZEV AZ CEeARLTWHS. © | excess risk indicate that higher risks are associated with
DlEMIL YH, KPEILIVLEL 0 WER IC EASA AZ ~~ younger age at exposure. Other analyses (not shown) indi-
PEERS LMA POTS. cate that females have somewhat higher risks of cancer
from radiation exposure than males do.
Late Radiation Effects KHGORZS [fl
BU 4. 1 Gy BeMEIC £ SED A DIRE VX 7 1 REF BRIE tt Ze S OVC BYE FO BE"? Fe BME
IB AUAXT VX Z (ERR), A BUSH RMX XZ (EAR) ICL BRA.
Figure 4. Effects of age at exposure and attained age on the excess risk of solid cancer (incidence) following expo-
sure to 1 Gy.'° Left panel represents excess relative risk (ERR) and the right panel excess absolute risk (EAR).
4
Acta Res FE Bh
Age at exposure
wo
1 GyS4EY ORI AD
Excess relative risk at 1 Gy
nN
0 i T r T
20 40 60 80
BIE im (ak)
Attained age (years)
ry fii, BPR. ARG. REE. FLBB. SNE FRIKIR, BZ
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OSLNCWA. Mary PILARCHASA Dit ClLRWPD,
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(63 fl), BLOW (54 PI) CHoK.
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Attained age (years)
Significant excess risks are seen for many of the major
types of solid cancer, including cancers of the stomach,
lung, liver, colon, bladder, breast, ovary, thyroid, and skin.
Although not always statistically significant, excess risks
are also seen for most other types of cancer. Thus, the sur-
vivor data are consistent with the notion that radiation is
associated with excess risks for virtually all cancers. Since
site-specific risks can differ by sex and age at exposure,
Figure 5 adjusts for such differences and compares risks
among sites by presenting sex-averaged data showing the
risk at age 70 after exposure at 30 years of age. Under
these conditions, the excess relative risk value (ERR) for
all solid cancers combined is 47% following exposure to 1
Gy. While differences in site-specific risks are apparent,
the range of variation is not statistically significant, partly
because the numbers of cancer cases at given sites are
limited.
Figure 6 presents similar site-specific data in terms of
attributable risk (i.e., what percent of total cases are associ-
ated with radiation). The largest excess number of cases
(given in parentheses) were for cancers of the stomach
(150), female breast (147), lung (117), rectum (78), thy-
roid (63), and liver (54).
Analyses of site-specific cancer incidence data are
often superior to those of cancer mortality studies. This is
because incidence studies provide better diagnostic infor-
mation and are better able to assess the occurrence of less
fatal cancers, such as thyroid and skin. For all solid cancers
combined, the excess relative risks were comparable
for incidence (47% excess per Gy) and mortality (42%),
but the excess absolute risk was 1.9 times greater (52
versus 27 excess cases per 10,000 person-years per Gy,
respectively).
Wh) HHROBWS Late Radiation Effects
5. LSS RHIC BF 3 BERENEE tit 30 i (BKFID) OAD 70 EIT L72NFO I Gy 4729 O
BBCI AA RAE OAS XZ BEBE 90% HE Ae RT.
Figure 5. Excess relative risk per Gy for the incidence of site-specific cancers in the LSS cohort. The risk is
standardized as exposure at 30 years of age (sex-averaged) and diagnosed at age 70.
The horizontal bars indicate 90% confidence intervals.’
4/H1720\A All solid cancer
ASB Bladder
XtEFLE Female breast
fifi Lung
fi Brain
FAAKER Thyroid
#8 Colon
#38 Esophagus
SNS Ovary
& Stomach
ET fi Liver
fiefs Pancreas
iB Rectum
ig (2 iB2RR<) Non-melanoma skin
+ Uterus
AU IZER Prostate
0.0 0.5 1.0 1.5 2.0
1 GySEY ORAZ
Excess relative risk at 1 Gy
6. BEBEHE (20.005 Gy) ICE CE MMHODATEAE, 1958-1998 2. A DEBAA BGR BB IC ED
RICA CEH DNS SO.
Figure 6. Number of site-specific cancer cases occurring in the exposed group (20.005 Gy), 1958-1998.
The white portion indicates excess cases associated with radiation.’”
f& Stomach
fifi Lung
AT iit Liver
+ Uterus
RB Rectum
fiz fist Pancreas
#38 Esophagus
AB Gallbladder
XtEFLE Female breast
5S Ovary
FSA Bladder
BIIZER Prostate
FAK AR Thyroid
Ai /R4R4HHE Brain CNS
R058 Oral cavity/pharynx
Biz Renal
Bile (iB &BR<) Non-melanoma skin
~€Mtth Others
0 500 1,000 1,500 2,000
FE PBX
Number of cases
Ai '419
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EL FEAL (|
1950 46.0 [| Aad HE % JE |
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DEABEDO 5ILTWRA (
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Late Radiation Effects KHGORZS fl
Leukemia™*
Excess leukemia was the earliest delayed effect of
radiation exposure seen in A-bomb survivors. Japanese
physician Takuso Yamawaki in Hiroshima first noted an
increase of leukemia cases in his clinical practice in the
late 1940s. This led to the establishment of a registry of leu-
kemia and related disorders and to the initial reports on ele-
vated leukemia risks published in the early 1950s.
Risks for radiation-induced leukemia differ in two
major respects from those for most solid cancers. First,
radiation causes a larger percent increase in leukemia rates
(but a smaller number of cases since leukemia is relatively
rare, even in heavily exposed survivors), and second, the
increase appears sooner after exposure, especially in chil-
dren. The excess leukemias began appearing about two
years after radiation exposure, and the excess peaked at
about 6-8 years after exposure. Today, little if any excess
of leukemia is occurring.
Because the LSS cohort was based on the 1950
national census, quantitative descriptions of leukemia risks
in A-bomb survivors have been based on cases diagnosed
from that year on. As of the year 2000, there were 204 leu-
kemia deaths among 49,204 LSS survivors with a bone
marrow dose of at least 0.005 Gy, an excess of 94 cases
(46%) attributable to A-bomb radiation (Table 4). In con-
trast to dose-response patterns for other cancers, that for
leukemia appears to be nonlinear; low doses may be less
effective than would be predicted by a simple linear dose
response. Even for doses in the 0.2 to 0.5 Gy range, how-
ever, risk is elevated (Figure 7).
24. LSS HM CBF S FUMIE E SHC OMB E HEEL, 1950 - 2000 4 1
Table 4. Observed and estimated excess number of leukemia deaths
in LSS population, 1950-2000"
Heaths Le eB anise
Weighted marrow dose WRAL LEE EL HEE eA BL a 28
(Gy) Subjects Observed Estimated excess Attributable risk
0.005-0.1 30,387 69 4 6%
0.1-0.2 5,841 14 5 36%
0.2-0.5 6,304 Pall 10 37%
0.5-1.0 3,963 30 tS) 63%
1.0-2.0 Le 39 28 72%
>2.0 737 25 28 100%
fat Total 49,204 204 94 46%
Wh RHO BRS Late Radiation Effects
7. DS02 —€ DSS ITLAAMIBD) LNG RX bU » Z Hse, 1950 — 2000 *F.
BERBIEE tit 20 — 39 EDAD 1970 FIZBIFSEBRPFHY KF"
Figure 7. DS02 and DS86 non-parametric dose response of leukemia, 1950-2000.
Shown is the sex-averaged risk in 1970 for exposure age 20-39."
10
8
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xR >
za 4 — - vse
eS 6
a] S
So
SN, dee
we 4
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0
BATITLEBHERE (Gy)
Weighted marrow dose (Gy)
*PY = J4F, CO CE ITE4EY LAA SE Y OE A UE PIELER
*PY = person-years, in this case the number of excess leukemias per 10,000 persons per year
8. BBIFERG Ze 5 OIC BIER £ SBA MAIC RM XZ) ORF (1 Gy BROW A)”
Figure 8. Effects of age at exposure and attained age on the excess deaths from
all types of leukemia (1-Gy exposure)"
8
1BAFGySEY OWFIC HR
Excess deaths per 10,000 PY-Gy
&
ee Efi
Age at exposure
Lss Mic bv Clk, BEB LOBHO FE HE A MG &
MEY VERMEER O AIL AZ OVID FD STV
Bo MAT ANAL ALG CREME CLARE CHE ET ADS
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Wes (PG a ER & (LAR CHPHR AIS AAS CLS HB Ic E 1)
ILILY AY OAR IMLID SNTORWY. IBRBAO
FVEY AZ ERIC. AIO ZAY AZ > EERIE
clk
BEF (mm)
Attained age (years)
Leukemia risk among LSS survivors has been
increased only for acute and chronic myelocytic leukemias
and for acute lymphocytic leukemia. No evidence of
increased risk is seen for adult T-cell leukemia (endemic in
Nagasaki but virtually non-existent in Hiroshima) or for
chronic lymphocytic leukemia, which, in marked contrast
to western countries, is extremely rare in Japan. As in solid
cancer risks, the leukemia risk also largely depends on the
age at exposure (Figure 8). The different age effect
WICKS CHOBE SITS (8). FROM IC Lo CAM
WOIATIASHODSH) . AME VONSIEERE A MS
RILS < LON SAS, Wes LOVER BEE Ug IS
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FA MME 11 HEB EOC. URE O FET A 7 Ik
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TASLFACH So. CMICK LT, LSS IS BITS 0.005
Gy DEORE e SIRE CHauettae 0.2 Gy)
AVE ALM AZ (S89 10 BIL/ FA ERT A 7 (EK 1.5)
Ch.
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FEPEC Ze EG (BR VENEUR) (ORS S VERTU RO gt
lk, (EEA LOA) ER AE (AHS) D5 1R56 NT
WS. FURR, BIALKIR, HERS LOPE O BE,
BOEUICA ORY —PILOW CHEAT ON TRIS. WH
Oty GS \< > HUN RE CO RMADSIED 67. CHE LK
FRAIC. PEO ON IEE O PAW PAE Old, VER
BIB O PDGF IRD OND, SNM
ldhhonepoks FHO RENE IC BV CHI 6 De ite
BUDE LO ILANT . PUREED 1 Gy Din FOAM A
FIZ 15 (95% fai 1.27-1.70) CHS.
Late Radiation Effects KHGORZS fl
involves different types of leukemias; acute lymphoblastic
leukemia is more common among young people whereas
chronic myelogenous leukemia and acute myelogenous
leukemia are more common among elderly people.
Because leukemia is a rare disease, the absolute num-
ber of leukemia cases among A-bomb survivors is rela-
tively small even though the relative risk is high. Leukemia
accounts for only about 3% of all cancer deaths and fewer
than 1% of all deaths, although it presently constitutes
about 16% of all excess LSS cancer deaths from radiation
exposure. In an unexposed Japanese population, the life-
time risk of leukemia is about seven cases per 1,000 peo-
ple. For typical survivors in the LSS, who received 0.005
Gy or greater (a mean dose of about 0.2 Gy), the lifetime
leukemia risk increases to about 10 cases per 1,000 (or the
relative risk is nearly 1.5).
Benign Tumors'*!
Information about the influence of A-bomb radiation
on non-malignant, or benign, tumors comes mostly from
research in the clinical Adult Health Study (AHS). Studies
have been conducted with respect to benign thyroid, para-
thyroid, salivary gland and uterine tumors, and gastric pol-
yps. In each case, a relationship to radiation dose was seen.
In contrast, no clear excess of pathologically-confirmed
benign ovarian tumors was seen except for sex-cord stro-
mal tumors. Figure 9 shows a distinct radiation dose-
response relationship for benign uterine tumors. The rela-
tive risk value at 1 Gy is 1.5 (95% confidence interval:
1.27-1.70).
9. FEBMOHMU AD BEE), AHS, 1958 - 1998 4201 KRIE 95% 13 FARE RF 0
Figure 9. Relative risk by radiation dose for uterine myomata, AHS, 1958-1998.'”
The dotted lines indicate 95% confidence bounds.
HU AD
Relative risk
2 3 4
BAtItTLEFBReE (Gy)
Weighted uterine dose (Gy)
Wh) HHROBLS Late Radiation Effects
10 (lathe MEERA IC BUT BIRR BE TOE (GE
(cA PERU RII ICL) DATES Y & i RRUR
BLOM CORRES. siti: 1 Gy 400
SHEP A bth AiR BlL, WHR LIER L TC 4 fF (95%
(BRAK 1.7-14.0) Ro CWS. ARO MMS, HC
FP WORE IC BV CHEE CH Ko
Figure 10 shows AHS prevalence data for hyperpara-
thyroidism (caused mainly by benign parathyroid tumors)
in relation to radiation exposure and age ATB. The preva-
lence at a 1-Gy tissue dose for all cases combined was four
times greater than for controls (95% confidence interval:
1.7-14.0). The prevalence increase was particularly
marked for persons who were children ATB.
10. AHS €HIZBIFS 1 Gy OBR PRIZE LEGG OF FARRAR RE TT IEE AWE (BERET mney) 1°
Figure 10. Prevalence of hyperparathyroidism, AHS, at 1 Gy radiation dose, by age ATB””
BiBO te
Prevalence ratio (log scale)
10
PLIERS © Few (ise)
Age at the bombing
30
PALDADRBIC KSECo"”
LSS HUF — ¥ (1950-1997 42) OFFICE YL DA
DORIC LSE Ae bie & FEC CRT HY I AR
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ISBROENTILYBWVYEF CHS. DS86 Hi iML2S 0.005 Gy
DLE® 49,114 KOH, 18,049 ABABA DIOKUE CE ¢
RoTwA (MIB IC EAU CIECORICGENTWIR
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MRE & BRK DA LAORBIC LARC OP CHUN
PERICLES Se Abi 4 RICE ARIE. 150 PID 5 300
BIE HET RW TV3S. 0.2 Gy PRL DS 0.005 Gy LLEO
HIRE 49,114 OFS tiie) ORNL SIEAILBITS
FOUL BIL, HOMER EK YW 3% MOTHS, CN
(LEIA AOL INZS (30 we CHE Lc. HELEC 7%,
EVE 12%) EHS TRY EDNCHS. COMB
ISOTBIRIZOV> TLE CH S (M11).
Tn,
¢
100 1,000
Non-cancer Disease Mortality?”
Analyses of LSS mortality data (1950-1997) show a
statistically significant dose-response pattern for death
from diseases other than cancer. The excess does not seem
limited to any particular disease. Among the 49,114 LSS
survivors with colon doses of at least 0.005 Gy (DS86),
18,049 non-cancer deaths occurred (excluding deaths
attributed to diseases of the blood). Circulatory diseases
account for nearly 60% of these deaths, with digestive
diseases, including liver diseases, and respiratory diseases
accounting for about 15% and 10%, respectively.
Aside from diseases of the blood, the number of excess
non-cancer deaths associated with A-bomb exposure is
estimated at 150 to 300 cases. The death rate following
exposure to 0.2 Gy (the mean radiation dose for the 49,114
survivors with doses >0.005 Gy) is increased by about 3%
over normal rates. This is less than the death rate increase
for solid cancers, where corresponding increases are 7% in
men and 12% in women (age 30 ATB). The dose-response
pattern is still quite uncertain (Figure 11).
Late Radiation Effects KHGORZS fl
11. 1968 -— 1997 FOMMEIZIV CORBA LHORE OD Bt IE BIER (DS86) 0° FERE CAR L 72 RRIL, BERBIEE Bit
Ved Br (LAVEE MBC LS AEA O Ze OBE ERR CF VERLTHIS. KLAR DW ERR HEE TC
BY, FRCL 72 HBL 5 F972 FICHE MAF 7 DERUISSAAACHEE MEK OU TO 1 BRE RZED
ERBBEOPRERT 2 ARMLREIIE MEO BULEBD & EO PRIICIN LZ BE DOCHS.
Figure 11. Non-cancer dose-response function for the period 1968-1997 (DS86).° The solid straight line indicates the
fitted linear ERR model without any effect modification by age at exposure, sex or attained age. The points
are dose category-specific ERR estimates, the solid curve is a smoothed estimate derived from the points,
and the dashed lines indicate upper and lower one-standard-error bounds on the smoothed estimate.
The right panel shows the low-dose portion of the dose-response function in more detail.
0.6
o
ns
RIX VAD
Excess relative risk
[-)
NO
0.0 05 1.0
1.5 20 25 3.0
0.2
0.1
0.75 1.00
BATHIT LEHR (Gy)
Weighted colon dose (Gy)
BALAN MBP BIS Ek SPEEIL OMT } AC RE &
NBER SNTHIS. COLIBRBICHL Tit
FEA OD MLO REPENS ELA DS A HETK & ER LT SD
SLNBWO CRMC AZ L 7. PARA AFCA If
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MOISE LEAS), CNODRAICL ) CORRE SAIL
MHT4ZOEICARPOK.
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BORCHERS. FREE (Bl 2 ISEB TS). BEEF
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al
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YN
A significant radiation dose-response pattern was also
seen for non-cancer blood diseases. Such diseases were
studied separately since they may represent various hema-
tologic malignant or premalignant conditions. Among the
128 deaths for which medical records were available and
in which hematologic reviews were performed, about 45%
were clearly classified as non-neoplastic blood diseases,
6% were diagnosed as leukemia or other hematopoietic
cancers, and the remainder were potentially preneoplastic.
In the absence of known biological mechanisms, it is
important to consider whether these results might be due to
biases or to diagnostic misclassification of cancer deaths.
Investigations have suggested that neither of these factors
can fully explain the findings, especially for circulatory
diseases that have been investigated more fully.
AHS incidence studies of non-cancer diseases show
relationships with A-bomb dose for benign uterine tumors,
thyroid disease (e.g., thyroid nodules'®), chronic liver
disease, cataract, and hypertension (Figure 12). The LSS
mortality data also show dose-related excesses for respira-
tory diseases, stroke, and heart diseases (Figure 13).
Wh) HHROBLS Late Radiation Effects
12. BEEBE 1 Gy D AHS HRA ICBITS BA LIAOREBA OM Y XZ (1958 — 1998 4) 17
Figure 12. Relative risk for AHS incidence of non-cancer diseases at 1-Gy exposure (1958-1998)"”
+ = Hie Uterine myoma
FAK ARES Thyroid disease
Bik: PREG Calculus of kidney and ureter
Z850u£ Dementia
(StEHRBSEKUBE Chronic liver disease and cirrhosis
11542 Myocardial infarction
FAKE Cataract
AMZ Stroke
KABA Aortic aneurysm
MIME Hypertension
MIMEtt DB Hypertensive heart disease
8% Gastric ulcer
\—+L VV 3R Parkinson’s disease
4A] Glaucoma
0.75 1.00 1.25 1.50 1.75 2.00
1 GySRUOHEMMUAD
Estimated relative risk at 1 Gy
B13. LSSRAICBIFSBALDMORIC LEH COMM AZ. AF TI —-B HSWVILLMPE, PAEH
WEBER, TAGE ClABATIICAEIC YU XZ DIMI TOS. BEBE 90% TAHA ERT 0?
Figure 13. Excess risk of mortality in the LSS due to non-cancer diseases. The increase is statistically
significant for all non-cancer diseases, or specifically heart diseases, stroke, respiratory diseases,
and digestive diseases. The horizontal bars indicate 90% confidence intervals.?
RAUNDTATORB
All non-cancer diseases
IRB
Heart diseases
AZA cp
Stroke
Ma eS
Respiratory diseases
Albee RB
Digestive diseases
RRB
Infectious diseases
EOWHORE
Other diseases
-0.2 0.0 0.2 0.4 0.6 0.8 1.0
1 GySKY ORIN UAD
Excess relative risk at 1 Gy
LSS AIO LBC KAP P— 9 Db, WOE
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EMMIBENTW4A. fEoT. AHS HRT ¥ BLEU LSS
FORA LO BR RICE BUS) Ic BIT Sy
Although the LSS data on heart disease mortality sug-
gest that radiation is associated mainly with hypertensive
and congestive heart disease, AHS data also suggest an
association with myocardial infarction, as well as with a
measure of atherosclerosis (aortic arch calcification).
There is particular evidence, therefore, from both AHS
clinical data and LSS mortality studies, that the rates of car-
Vib MS BO FEARS ASAI LCS E (LIEIZPAME CH So
LD EF CARO IE L Le BA AEMEO dy HE WENO RIE IC
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Late Radiation Effects KHGORZE fl
diovascular disease are increased in A-bomb survivors,
especially, it appears, for persons exposed at young ages.
Studies regarding possible underlying biological mecha-
nisms are being conducted.
Chromosome Aberrations”? *”
Chromosomes are composed of long thin molecules of
DNA. When cells are exposed to radiation or carcinogens,
DNA sometimes breaks, and the broken ends may rejoin in
different patterns from their original arrangement. The
abnormalities that result are termed “chromosome aberra-
tions” and may be visualized at mitosis when cells divide.
The frequency of chromosome aberrations increases
with radiation dose to the cells and serves as an indicator of
radiation dose received, i.e., a biological dosimeter. In
vitro irradiation experiments using blood lymphocytes can
provide a dose-response relationship that can be used to
estimate radiation dose to individuals on the basis of the
aberration frequency detected in their lymphocytes.
Among different types of aberrations, dicentric chro-
mosomes are relatively easy to detect, and their frequency
is therefore useful as a biological dosimeter. However,
dicentric frequency declines within a few years because
the presence of two centromeres in one chromosome inter-
feres with cell division. Thus, the frequency of dicentric
chromosomes can be applied to recent exposure cases
only. Since A-bomb survivors were exposed to radiation
many years ago, dicentric frequency is no longer useful for
biodosimetry, and the frequency of translocations (and
inversions) is used instead. Such aberrations have a single
centromere per chromosome and hence can divide so that
the altered chromosome persists for many years. However,
they were more difficult to detect by conventional staining
methods.
Figure 14 shows the relation between DS86 dose and
the mean fraction of cells with aberrations (mainly translo-
cations) measured by conventional staining in survivors
exposed in typical Japanese houses in Hiroshima and
Nagasaki. The small but consistent differences between
the two cities may be due either to different scoring effi-
ciency of aberrations in the two laboratories or to differen-
tial errors in DS86 dose assignments.
Currently, chromosome studies for survivors in both
cities are examined solely in the Hiroshima laboratory,
using a modern chromosome painting method (fluorescence
in situ hybridization [FISH]). Chromosomes 1, 2, and 4 are
stained yellow and other chromosomes red so that translo-
cations between yellow and red chromosomes can be
detected unambiguously (Figure 15). The FISH technique
has made translocation detection easier and more accurate
and has been used successfully in studies of radiation expo-
sure accidents, such as Chernobyl.
Although fetuses had been regarded as radiosensitive,
chromosome aberration data for survivors irradiated in
Wh) HHROBLS Late Radiation Effects
14. AHS HARB ABET OREM CAF SMOG & Bid & OBR
Figure 14. Relationship between fraction of cells with chromosome aberrations and radiation dose to
AHS survivors exposed in typical Japanese houses
30
20 Ds
Hiroshima
y
=
d
“Bell
:
Nagasaki
10
Percent of cells with aberrations
LERRE EH OMMOZIS (%)
0.0 0.5 1.0 ies) 2.0 2.5
BAILA BRE (Gy)
Weighted marrow dose (Gy)
15. #06 in situ7\4 FU YA C-Y a VE CHRMSENRAR AAA. A7CBRULIE RS
FIBRE (KE) BAF.
Figure 15. Metaphases labeled with fluorescence in situ hybridization (FISH). The left metaphase shows
a normal cell and the right, a translocation indicated by arrows.
Fa VAIS RIC L CRED LEZ SU TAHRAS
JAN BRIERE OF ARREICE TS 7-4 (40 eH fe CO IL
BY YONERB) > 5 (SCN O BEL BIR S RPO Ko
VIA Ho TRC b, BOIS IS EER BA Lb Ne
DS, JAVEHAIC IRR SNL A 20 IC MNEIG GLE
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PHPRIC BU SAAMI OM) (CAR RE DRS
NTR4ONCULRVPEBHDNE. FOC. MMH &
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BIVSAVATAUY A (GPA) GIRS ORAB RMS
ROME DSIRE SNORT EAH SG Ale LAL
GPA ifn FFA EAMES, CIC BE LC tes
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HOST MN OM AAAS RAGE SIERO, MED (HS
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Late Radiation Effects KHGORZS [fl
utero did not show a radiation effect when their blood lym-
phocytes were examined at about 40 years of age. A mouse
study also confirmed that chromosome aberrations were
not seen in offspring 20 weeks after in utero radiation
exposure, although they were seen in mothers after expo-
sure in adulthood.
Chromosome aberrations have been examined in
clonally derived cell populations in vivo (cells bearing an
identical aberration) to see if clones show an increased
level of additional aberrations, which would indicate they
have “genomic instability.” The results did not show an
increased rate of later aberrations indicative of genetic
instability.
Somatic Cell Mutations”? *"
As shown in the previous section, radiation effects on
chromosomes remain in lymphocytes even many years
after radiation exposure, and reflect effects on genetic
material contained in the chromosomal DNA. Therefore,
radiation effects on genes resulting in mutations in
“somatic cells” (all the cells of the body other than the
reproductive cells of the ovary or testes) were also
expected to remain in the body. Following tests of several
assay methods using blood cells, it was found that they did
not record dose effects except for mutation in the gly-
cophorin A (GPA) gene in red blood cells. The frequency
of GPA mutant cells, however, varied extensively among
ordinary people who were not exposed to radiation, which
prevented us from evaluating individual radiation dose
from the frequency. This observation is understandable if
we assume that, while the mutation induction rate is gener-
ally on the order of 10~ per Gy, the total number of long-
term stem cells in bone marrow would not be sufficiently
large, e.g., several 10°. Thus, the GPA test is not consid-
ered useful for individual dose evaluation but collective
dose of a group of people with similar exposures.
Immunity?2-°7
Immune cells are known to be vulnerable to radiation,
through induced apoptosis (programmed cell death) in
mature T and B lymphocytes (long-lived white blood cells
responsible for adaptive immunity) and by lethal damage
in bone marrow stem cell precursors of monocytes and
granulocytes (short-lived white blood cells responsible for
innate immunity) as well as natural killer cells (Iymphocytes
responsible for innate immunity).
In persons receiving heavy doses of A-bomb radiation,
both mature lymphocytes and bone marrow stem cells
were severely damaged, causing profound depletion of
granulocytes and natural killer cells, which together
) HHROBLS Late Radiation Effects
7 — MASI Lo SOR, BS OAMAS RGEC EY
RE LK.
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defend against microbial (or bacterial and viral) invasion.
As aresult, many people died from active infections.
About two months after exposure, marrow stem cells
recovered, and deaths due to infection generally ended.
Studies of survivors since the 1980s have shown no abnor-
malities in monocytes, granulocytes, and natural killer
cells, indicating that damage to innate immunity occurred
only during the early period following the bombings.
The recovery of CD4 helper-T lymphocytes (a major
subset of T lymphocytes responsible for antigen-specific
immunity) took longer, and studies have shown that CD4
T lymphocytes recovered only incompletely. Even today,
the relative number of CD4 T cells is, on average, 2%
lower per Gy. More in-depth studies have shown that
among those with higher radiation doses a greater propor-
tion of T cells are “memory” T cells rather than newly
formed naive T cells, indicating reduced ability of the
thymus to produce new T cells. In contrast to diminished
CD4 T-cell numbers and function, the number of B cells is
slightly higher in exposed persons, perhaps as a compensa-
tion. Tests show that CD4 T cells from high-dose persons
tend to have less reactivity to an infectious agent. Also, as
a compensation for decreased T-cell function, cells respon-
sible for innate immunity are activated and produce inflam-
matory proteins, and our studies have shown that persons
with higher radiation exposures have lower numbers of
CD4 T cells and elevated levels of various inflammatory
proteins in their blood. These trends parallel what is seen
with advancing age, suggesting that radiation exposure
may accelerate immune aging processes.
To date, there has been no clear evidence that any spe-
cific health effects have resulted from the persistent abnor-
malities observed in the T and B lymphocytes of A-bomb
survivors. The reason may be that wide variations in spe-
cific immune responses make it difficult to identify per-
sons with radiation-impaired immunity to specific patho-
gens. For example, in tuberculin testing for vaccination
against tuberculosis, some people show immediate posi-
tive results, and others do not. There is also no evidence of
radiation effects on risks for chronic infectious diseases,
such as tuberculosis, or autoimmune diseases, such as rheu-
matoid arthritis. On the other hand, a slight dose-related
decrease in immunity has been observed against certain
viral infections. For example, the proportion of people who
carry the hepatitis B virus increases by A-bomb dose.
Late Radiation Effects KHGORZE fl
Bete : EAR Physical Growth and Development®*°
ABCC —REAECIL, ECEHIEBOMEOKREE LH Body a Hanne
= = z , etc. t t 5
(RHE (ER. RE, WHEL) DRI CHbn | (Me ete have been taken a as indices 0
: __ growth in young A-bomb survivors. Findings show that
TE Ko ARORA, SEO BURN TREE IC LO BR growth retardation has been a general result of childhood
be
He eA CAC EDM SMicwzoTWS!. M16 (4) lki# | exposure to bomb radiation. Figure 16 (left) represents the
AWEROM EC. PEUEMLEDS 1 Gy HMO BEC (k BEBE IS HAE results of fetal exposure cases; while no clear dose effect
: ‘ ; es .; Was seen among those who were exposed to <1 Gy, larger
CRW ADS, 1 Gy WEL OH Cla AED FRILH 6 cm Di : ;
2 ? an Cone doses (21 Gy) did cause decreased adult height by about 6
DPSS 1 Gy BEY CEH 2.5 cm) o 10 MOK EC cm (or about 2.5 cm per Gy). The effect was already seen
FEI LO NAD, CORD EAOAROMO (LH | at age 10, but the subsequent pubertal growth spurt was not
BL Cute, P16 (4) lk, PR LEO AEDS RS affected. Figure 16 (right) represents the results of expo-
BADUMBERT LOC, 0KERECEHORMOME ue at various ages, which used ne first height informa-
: tion after age of 20 years. The radiation effect seems to be
EIA CV So BEL & REED HIRO GBD 9 7 5 more pronounced among females than in males. Studies
CHS. KHEO MMF tiI< BIS 4 HAS TD NLA, WN — were also conducted regarding age at menarche among
MORANABRO SNe Pok., LASLRTOF-—F7A51k, female survivors, but no radiation effects were seen.
Ss
HUM MUMEMEIZ kD PARRA E ZT ARMERRIB ANS Recent data, however, suggest a possibility that radiation
exposure has led to an earlier menopause.
E116. BHROKRIKCRIES OH. At, BABRAOGEO 10 wid 5 18 we BITS WER EDF 0
WEMNL GL, BEML HERE OE Bh? SERRLB BE O mGy DEBIT, WEIL 1-999 mGy #,
FUBRIE 1,000 mGy LE DEE (DS86 FER) © ARNT, BERREE RIC 1 Gy BIR OBB EAT 08
meh iL 1 Gy 4720 DAF RAOPBE (HILT cm), BAMITBHELTAFOF i. MANZE PAAR EMIS
BE WERRIS AS BRIEF t= 3 1F S 95% Ga RA Fl. BEBRIL ei EBRD 95% FHA I ENF
Figure 16. Radiation effects on height. Left panel indicates results on fetally exposed survivors measured at ages
from 10 to 18 years. The X-axis represents height and the Y-axis the age at the time of examination (ATE).°?
The solid line represents 0 mGy control subjects, dashed line 1-999 mGy group, and dotted line > 1,000 mGy
group (DS86 uterus dose). The right panel shows the effects of 1 Gy exposure at different ages®*. The
X-axis represents the age at exposure and the Y-axis the radiation effects in cm per Gy. Circles
represent females and squares males. Vertical bars indicate 95% confidence intervals (CI) at
various age ATB, and dashed lines 95% CI of the linear regression line.
170 3
Bt
Male ~S
160 RS
a ® att
= AE so Female
f= § 150 . Female Q€é
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a § ee | Seah
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120
110 =A
107 1 i213) 14, 15 16; 17> As 0 by 10 15 20
IE RRERR (RE) RAS ERG (iE)
Age ATE (years) Age ATB (years)
HAE 41-45 Aging***
HEV LERD O, HUME S12 Bea Animal experiments have shown that radiation expo-
sure shortens the lifespan. The results were once inter-
CBELERDP OWS. COMBMAIL, PO TILK é fog ae t
preted as being due to radiation-induced non-specific
SARIS LS IPA IE DUR O NEI LS LDEDBR — acceleration of aging, but later studies showed that tumor
DHOOM, TOROMEDS, Fearsswiolse A ithe | induction accounted for essentially all of the life
) HHROBLS Late Radiation Effects
PRIZED Lene eee nae
JSR DUES I< 38 1T S IPP RAY Ze DIME HE & AN EPL IE
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DUE TC dD 6
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PER UC BSE L Ze) BEE BOL OH ti D FE AE HG
1950 4E(C EE ICPEICH SIS SN TW. BLEEDS 0.005 Gy
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(0.8%) IC HREAPAGET DS LYE SNE OI LL. BREEDS
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PSE MH IQ TEELONR PDIBD SN (18). FEVEE
BOD 3639 Hl b BA Alc
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fTbrCTBY, CARIN AAPSAAA AMET SL,
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HURT O BRUTE CS. ERE IC BV TRAE (18
ine) ne {SEO AE TEHY Te DP DE SILT Ho IO
Ni
im
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BWR (ERR IE 1.7) ELEN CHARICE ADC
DH)
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shortening.
In studies of A-bomb survivors, there is little or no evi-
dence for non-specific accelerated aging in most physiol-
ogic parameters or morphologic effects (e.g., radiation
dose is unrelated to breathing capacity, ability to focus
vision, skin elasticity, grip strength, and hearing ability, or
to tissue differences at autopsy). However, radiation-
related increases are seen in the prevalence of cataract and
atherosclerosis, as well as in altered immune-inflammatory
serum protein levels. Continued data collection is neces-
sary to determine whether radiation exposure leads to non-
specific aging.
In Utero Exposure
Mental Retardation and Growth Impairment**
By the late 1950s, exposure-related increases in small
head size and mental retardation were noted in persons
exposed to radiation in utero. Severe mental retardation
has been diagnosed in 21 of 476 in utero survivors (4.4%)
whose doses were 0.005 Gy or greater compared with nine
of 1,068 (0.8%) whose doses were below 0.005 Gy. The
prevalence was strongly associated with radiation dose and
gestational age (1.e., particular developmental stages)
ATB. Excess mental retardation was especially
pronounced in persons exposed at 8 to 15 weeks after
conception, and to a lesser extent among those exposed at
16-25 weeks, but no excess was seen after exposure at 0-7
weeks or 26-40 weeks after conception (Figure 17). Dose-
related decreases in school performance and IQ scores also
were observed among the 8—25 week groups of in utero
survivors, after excluding severely mentally retarded chil-
dren (Figure 18), and increased seizure disorders were also
evident in those groups.
Magnetic resonance imaging scans of the brains of six
severely retarded in utero survivors suggest that radiation
exposure during the third and fourth months of pregnancy
may result in distinctive physical abnormalities in brain
structure. As in persons exposed as children (Figure 16),
annual body measurements of survivors exposed in utero
have demonstrated an overall reduction in adult height and
weight by age 18 in the high-dose group. These effects do
not differ by sex or gestational age ATB.
Cancer Incidence*?”°
A recent analysis of cancer incidence at ages 12 to 55
compared data for survivors exposed in utero with those
exposed in early childhood. For the in utero survivors there
was a significant dose response with an excess relative risk
(ERR) of 1.0 per Gy, a risk not significantly less than that
for survivors exposed during the first five years of life
(ERR = 1.7). However, the temporal patterns of the excess
absolute rates which increased rapidly with age for early-
sie
7234
TEV
ta
AD
HOT EDS UE ST AZ OWA LC. RAPER CIEE FL
FAOMMA Lonewv kj Chok. RELMHO
Id, BURR CldHATHIICA EE CILE V3. PRC EB,
PRICE AMR MMOBAY AZ ASSAM IS EY
CMAN CE Le CE DHE LCR ZACH4AI.
Late Radiation Effects KHROBRS I
childhood exposures did not increase following in utero
exposure, but the difference between the two was not statis-
tically significant at this time. It can at least be concluded
that adult cancer risk from in utero exposure is not greater
than that from early childhood exposure.
17. HEAR IA BUT S Beit © Ne PLL a HY D BEG ALE He *7
Figure 17. Severe mental retardation by radiation dose and gestational age among A-bomb
survivors exposed in utero
BSE A (%)
Risk of severe mental retardation (%)
0 0.10 0.20 0.30 0.50
47
8-15 JAR
8-15 weeks
16-25 iB
16-25 weeks
1.00 1.50
BAT lt LEAT E ERE (Gy)
Weighted uterine dose (Gy)
18. RABE ICBITS FEM (DS86) BL OAM AFIY 1Q FREE 95% fa
Figure 18. Mean IQ scores and 95% confidence limits by uterine radiation dose (DS86) and
gestational age among A-bomb survivors exposed in utero’
130
120
° . ;
#5 110
1 3 "Or st 9 I re.
S2 t99 |
8
= 190
80 t-OH xt FB# Control (<0.01 Gy)
+@4 0.01-0.09
= La 0.10-0.49
Lv 0.50-0.99
HOH >1 Gy
Fae 0-7 8-15 16-25 264
age SAAB OD ELIS
Age in weeks after conception
Wh) HHROW NZS Genetic Effects
RHRO ahs =
EE AERCN LD HEME DAE SAMO DNA (cf (Ze
GAR OTL, GEMRKOUK (F)) ea,
(owt LC PRAMS AEC RARE RIL ROU Ic fab S
TENE,
Eb OARS AM LEIA FEAR EEL, RC Ekipibe C I BEC
bd. isles i mn CRRA Ze EE
CHHAERPRE SS ee MRT eC) DH CSAS, CHETOL
= JERE @ Ff CHRIS E Ze VA VERE NY Ze OBE & AE Ze
EVI PELL SITY. TBIO FSB DIB
{RVC PRURMEEE O ORAIL CPEB % 1c 0.14 Gy)
RBIS TUL, COMRILE SAAC E CLE, BECO
AV ARAWLERDSOFUN ERLE) TEENY
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#65 (clk 1940 EHR A 5 ABCC — HiT CE LT &
7 ERB OF HEISE T SROMPOU MELAS . Hh
PRE Be)
TEx F, RA OPEC IMA AE MET SEE BIC, Fy HARE
Kenran. PekRe ce CO FED 5 tet S 17 MHLO DNA
VS CHE BAP EU SIV ORE TOTS,
Genetic Effects
When ionizing radiation causes DNA damage
(mutations) in male or female reproductive (“germ’’) cells,
that damage can be transmitted to the next generation (F)).
This is in contrast to mutations in somatic cells, which are
not transmitted.
Detection of human germ cell mutations is difficult,
especially at low doses. While high doses in experimental
animals can cause various disorders in offspring (birth
defects, chromosome aberrations, etc.), no evidence of
clinical or subclinical effects has yet been seen in children
of A-bomb survivors. Given the relatively low average
dose to survivors (median doses of about 0.14 Gy for both
the fathers and mothers), this result is not surprising. It is
consistent, in fact, with the predictions of mouse experi-
ments and suggests that humans are not more radiosensi-
tive with respect to heritable changes.
Table 5 lists the several kinds of genetics studies con-
ducted at ABCC-REREF since the late 1940s in children of
A-bomb survivors. Active studies involve ongoing mortal-
ity follow-up of the F, cohort, an F, clinical examination
program, and various molecular studies of DNA from cells
of survivors and their children.
#5. ABCC — WGPWZ BUT BIERERIET OD FEO te ANY APE
Table 5. ABCC-RERF genetic studies of children of A-bomb survivors
al I Al
Studies
HAERPSe a GCRE. IGHESE HH ze XC)
Birth defects (stillbirth, malformation, etc.)
{KE Weight
}EIE Sex ratio
Ye ff ($524 Chromosome aberrations
48 A/S Sk 8) Protein electrophoresis
FOE, DSA FBAZS Gitte)
Mortality, Cancer incidence (ongoing)
a le sat
Clinical examination program
DNA wl #e (AikiCHF)
DNA studies (ongoing)
HAE RE RES (1948—1954 4) 51—54
ERWURE OF HEC BU SB HERBS ¥ ELE OF
DUE Wr RR ES Dea CA CBM L 7 EVs 9 SSE LEB
MONT. Keg RMPOIET A CORAM S
MAAS 1948 AEC AAA ST 6 ELV COR HTA
76,626 AAS, ABCC ORM LABGRe LIK. HAD
EAD AFK
Population size
77,000
72,000
141,000
16,000
24,000
77,000
12,000
1,000 Zhe families
(1,500 ,O-+fE offspring)
Birth Defects in F, Offspring (mainly 1948-
1954)°'-*4
No statistically significant increase in major birth
defects or other untoward pregnancy outcomes was seen
among children of survivors. Monitoring of nearly all preg-
nancies in Hiroshima and Nagasaki began in 1948 and con-
tinued for six years. During that period, 76,626 newborn
Wa S17 ARO AA CIS, RED BEIT OVC ACG HB DS
FROM TW PAS, 20 ALLE O KEM COV CSE BI ALPS
Hook, COPPA B HI CREST STHRICBOV CC,
THIS BU A RAED 90% DLE ASMERE S 1 TERRE EEO
BALD SA HEC Ro
HAR 2AM UA PAO BSBIck YO. HAR MAT,
ROVE, VE. PAVWIOME, BLOLER MARE
LOU CHRO 5 N17. TURRET. ALO
BE % PLO Pest BIC 6. 7, SICAT. AAAI MRED
Ze VT BLA 5 AEE IL. JIT OH 3 7% 65,431 ADHD
BAK HV HAE PEE EAE BS (594 PI, 0.91% (2424) Id,
HO AR + EERE CHP NK ARADO WEIS SARL
Ha EO RM RE -RL CWA. COMBE CHES 17 HE
(AR REE CIS ADS Ze APS, 0.92% ILFHBAILS TVs
Bo CORIO HURST b BLO BUN iia E 7 (SME
ORRe AR SB POK.
OS (HBO OAC HARE IL, ARIE, OR,
RA (ARBRE CE ODER CLE OSS). ARE,
Sisie (POPS 5 ARES SK) BLOGHHE (248
DhLORAIKIE) Chok. CNS5ORHIL, H8 OI
YA 594 OF 5D 445 Kh (75%) IHD SNK.
HH AE Fee ESE OD HEL, RIC SER EC ESE Ze EO EF Uc
PAE VAMC ILFEL LBV BE OBHAODC. HRS AAMDS
107 A AIRED bin. HARE Sit 7 FH 18,876
AM7 By 378 KA (2.00%) IL -OYED HV BEE DSW 5
nko CILLBHOMEIL, AR 2 AADADRE CIS
0.97% Chek. COCO MO RERH tie ¢ OR REEL
WHRENRPokK. KAK Ro CTHNARERHADSL
% FEO 72 Fy HARE ARDY T A172. 2008 “E 8 ABEL tix
4) D CASE HE (Radiation Research 2008; 170) CHA.
Fe 6. JR BETTIS BUT 3 MEER BPE,
Genetic Effects KHROWGHRS
infants were examined by ABCC physicians. When
surveillance began, certain dietary staples were rationed in
Japan, but ration regulations made special provision for
women who were at least 20 weeks pregnant. This supple-
mentary ration registration process enabled the identifica-
tion of more than 90% of all pregnancies and the subse-
quent examination of birth outcomes.
Physical examination of newborns during the first two
weeks after birth provided information on birth weight,
prematurity, sex ratio, neonatal deaths, and major birth
defects. Newborn frequencies of untoward pregnancy out-
comes, stillbirths, and malformations are shown in Tables
6, 7, and 8 according to parental dose or exposure. The
incidence of major birth defects (594 cases or 0.91%)
among the 65,431 registered pregnancy terminations for
which parents were not biologically related accords well
with a large series of contemporary Japanese births at the
Tokyo Red Cross Maternity Hospital, where radiation
exposure was not involved and overall malformation fre-
quency was 0.92%. No untoward outcome showed any
relation to parental radiation dose or exposure.
The most common defects seen at birth were anen-
cephaly, cleft palate, cleft lip with or without cleft palate,
club foot, polydactyly (additional finger or toe), and syn-
dactyly (fusion of two or more fingers or toes). These
abnormalities accounted for 445 of the 594 (75%) mal-
formed infants in Table 8.
Since many birth defects, especially congenital heart
disease, are not detected in the neonatal period, repeat
examinations were conducted at age eight to ten months.
Among the 18,876 children re-examined at that age, 378
had one or more major birth defect (2.00%), compared
with 0.97% within two weeks of birth. Again, there was no
evidence of relationships to radiation dose. To avoid over-
looking the adult-onset diseases, an F, clinical health sur-
vey was conducted during 2002 to 2006 which focused on
lifestyle diseases. The first report is in press (Radiation
Research 2008; 170) as of August 2008.
WE. HAR 2 AHMUADEL) OELD
(BOWIN, SEB HIES 172-LHKOR, 1948 - 1953 4f)?
Table 6. Untoward pregnancy outcomes (stillbirths, malformations, and neonatal deaths
within two weeks of birth) among
A-bomb survivors, by parental
radiation doses and cases/children examined, 1948-1953°°
EESLO Hathlt LEBER RHOBAH I L cist Father’s weighted dose (Gy)
Mother’s weighted dose (Gy) <0.01 0.01-0.49 20.50
<0.01 2,257/45,234 81/1,614 29/506
(5.0%) (5.0%) (5.7%)
0.01-0.49 260/5,445 54/1,171 6/133
(4.8%) (4.6%) (4.5%)
20.50 63/1,039 3/73 7/88
(6.1%) (4.1%) (8.0%)
) RHHROW NZS Genetic Effects
#7.
VERE BERET NZ BUT B WERE HEPA WIFE ES 7172 FOR, 1948 - 1953 fF) °4
Table 7. Stillbirths to A-bomb survivors by cases/children examined, 1948-1953 *!
BEBO REEL
Mother’s exposure THA Ee
conditions Not in cities
HAASE 408/31,559
Not in cities (1.8%)
{EHP tat 279/17,452
Low to middle doses (1.6%)
Tue 26/1,656
High doses (1.6%)
RHO WREKIN Father’s exposure conditions
{EFF ae faye
Low to middle doses High doses
72/4,455 9/528
(1.6%) (1.7%)
139/7,881 13/608
(1.8%) (2.1%)
6/457 2/144
(1.3%) (1.4%)
B88. AEB 2 IAD BIS 17 IE SEN APES 7EL LE OR, 1948 - 1953 4f)*"
Table 8. Malformations diagnosed within two weeks of birth by cases/children
examined, 1948-1953 *!
EEBLO MERKUL
Mother’s exposure THA HE
conditions Not in cities
THA ASE 294/31,904
Not in cities (0.92%)
JERE ites 144/17,616
Low to middle doses (0.82%)
Bee 19/1,676
High doses (1.1%)
PIE (1948—1962 4) 55
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QPOR ENKI Father’s exposure conditions
{EEE le ie
Low to middle doses High doses
40/4,509 6/534
(0.89%) (1.1%)
79/7,970 5/614
(0.99%) (0.81%)
6/463 1/145
(1.3%) (0.7%)
Sex Ratio in F, Offspring (1948-1962)°°
In the past, lethal recessive mutations of the X chromo-
some were thought to alter the birth sex ratio in favor of
females if mothers were exposed to radiation, since the
single X chromosome in males is derived from mothers,
and in favor of males if fathers were exposed, since the
male X chromosome is transmitted only to daughters.
Early observations concerning births to A-bomb survivors
(1948-1953) favored this hypothesis but were not statisti-
cally significant. Further data collected through 1962
(140,542 births, 73,994 with one or both parents exposed)
did not support any radiation effect on sex ratios.
Subsequent considerations regarding errors in sex
chromosome number and patterns of X chromosome inacti-
vation in embryonic and extraembryonic tissues have
made it difficult to determine how X chromosome muta-
tions may affect sex ratios. Under these circumstances, it
seems doubtful that sex ratio measurements can be useful
as indicators of genetic radiation damage.
REAR (1967-1985 tf) 5657
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Genetic Effects KHROBGHRS fl
Chromosome Aberrations in F, Offspring
(1967-1985)5©57
Extensive chromosome analyses have been done in F;
offspring of A-bomb survivors to determine if radiation-
induced stable aberrations in parental germ cells
(reciprocal translocations and inversions). No evidence
was found to suggest increased F, aberrations.
Studies compared 8,322 persons with one or both par-
ents within 2,000 meters of the hypocenters (estimated
doses of 0.01 Gy or more) and 7,976 persons with parents
beyond 2,500 meters (doses less than 0.005 Gy) or not in
the cities ATB. Eighteen persons in the exposed group and
25 controls carried stable aberrations (Table 9). Tests of
parents and siblings showed that most aberrations were
pre-existing and inherited from one parent. Only one from
each group had a newly arisen aberration. The origin of
aberrations in 16 cases could not be determined because
parents had either died or did not wish to participate in the
study. Dose distributions, however, were similar in tested
and untested parents.
FE 9. JEBEL OD L-MELZ BUF B BERRA SE Hi O
Table 9. Stable chromosome aberrations in children of A-bomb survivors ™
RRR eR ORKFRON
Children with aberrations
SLD ee x} HRI Control group #xURHE Exposed group*
Origin of aberrations (7,976 \. children) (8,322 \. children)
ia 1 (0.01%) 1 (0.01%)
Newly arisen
TH BIO ES BASIC HK
Inherited from either parent I MC) ty OnE)
y a ST & Fa pxr >
Re ee 9 (0.11%) 7 (0.08%)
Parental origin untested
& at Total 25 (0.31%) 18 (0.22%)
* SJE at 0.60 Gy Mean dose 0.60 Gy
MREABORRER (1975—1985 sf) 8-6
1976 4F 4lkelk DNA D2VA BER & EADY -Y T
BEUINDEPOLOTC. MEH CILKOD 2 FED ZEKE SE
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FIZEIRIE SEC ho CHOA BAUM LO [En] PRIM
CRITE RAMEE AV CHS NZ ED CH OK. ft
FERRARA SER BA AE!
ChHokK.
Blood Protein Mutations in F, Offspring
(1975—1985)°s©°
In 1976, since no techniques were available for direct
screening of DNA mutations, RERF used two kinds of pro-
tein alterations as potential indicators of mutation. One
was a rare electrophoretic variant arising from base substi-
tution mutations and was detected by one-dimensional
electrophoresis. The other was an enzyme-deficient pro-
tein variant caused by deletion mutations.
Wh) HHROW NZS Genetic Effects
10 4A IC 70, LSS 4EBII
HOFLOE
- IR Ae ES
WEES LY RAEL (Zé 10),
IZOVWrT
11) ° POL i) ail AE ie a ae DS 0.01 Gy L
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pRIE SZ
Over ten years, nearly 24,000 children of LSS survi-
vors or controls were screened for electrophoretic variants
of 30 blood proteins (Table 10); 10,000 of these children
were also tested for enzyme-deficient variants (Table 11).
The children were classified into two groups according to
the combined parental gonadal dose of each child, either
0.01 Gy or greater (exposed group) or below 0.01 Gy
(control group). A total of 1,233 electrophoretic variants
and 47 enzyme-deficient variants were detected. Studies of
parents showed that most variants were pre-existing and
that only six electrophoretic variants and one enzyme-defi-
cient variant originated from new mutations in parental
germ cells. In the study of electrophoretic variants, two
new mutations were detected in the exposed group and
four in controls. The only enzyme-deficient mutant found
was in the exposed group.
2210. xt LBC S 3 Gt
Table 10. Results of screening for electrophoretic protein variants
mate Le HED Be
Children examined
Ewen Le wate FAL Leg
Loci tested
New mutations
(xt HaH Controls)
PIRES / TBF / TAC
<0.01 Gy 20.01 Gy*
(@kUETE Exposed)
12,297 11,364
589,506 544,779
4 2
0.7x 10° 0.4x 10°
Mutation rate/locus/generation
* BAIT Lee ieitite 0.49 Gy
* Weighted mean dose 0.49 Gy
#211. AERIGPEOI P LERMBBRC FS OR
Table 11. Results of screening for enzyme-deficient protein variants
<0.01 Gy
(xT ARE Controls)
20.01 Gy
wate Le HEO Re
Children examined
aa L ett EL
Loci tested
SERIE RIL
New mutations
PRB ER / TBE / TR
Mutation rate/locus/generation
(@kUETE Exposed)
5,026 4,989
61,741 60,529
0 1
0 2x10°
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fe (SFE BLY. HFOSCHAS ECICLS ¢ ORME
DBUBECHS)o CDI aAVFIA bhRERICGT 5H
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BU BLIC ER L 7 RR (7e72 L. BEUR ee IS ae k
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BUR OU ENHAEICELS S DNA HAL LC. REV
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Genetic Effects KHROWGHRS I
These results provide no evidence for radiation-
induced germ cell mutations. This may not be surprising
since the enzyme-deficiency study was too small for ade-
quate statistical power to detect radiation effects and since
it later became clear that radiation only rarely causes
altered base substitutions and hence altered electrophoretic
mobility. Direct screening for DNA mutations is now
being undertaken.
DNA Studies in F, Offspring (1985-present)®*©>
DNA studies of survivor families make use of Epstein-
Barr-virus transformed cell lines established from
peripheral blood B lymphocytes. Cells come from parents
and all available children of 1,000 families, 500 with one
or both parents exposed to doses of 0.01 Gy or greater and
500 with neither parent exposed to significant doses.
Uncultured lymphocytes and polymorphonuclear leuko-
cytes are also preserved. New techniques for DNA analy-
sis such as DNA chip technology are currently being
developed.
A pilot study has been initiated to examine DNA in
100 families, 50 exposed and 50 controls. Minisatellite
genes comprise high tandem repeats of core sequences
(more than a few base pairs), which are located at many
places in the genome, and are known as highly polymor-
phic in its repeat number (or total length). As such genes
are highly unstable in nature and the spontaneous mutation
rate is high, genetic effect of radiation can be detected with
tests of a relatively small number of offspring. The results
by eight probes and DNA fingerprints analysed by a multi-
locus probe, 33.15, are shown in Tables 12 and 13. No
effects attributable to radiation have yet been observed.
Among new mutations at minisatellite loci, more than 80%
are derived from male parents (the production of sperm
involves many times more cell divisions than that of eggs).
RERF results on the minisatellite mutations are in contrast
to the results obtained by an English group on radiation-
exposed families (but the exposed doses are much smaller
than those in A-bomb survivors) after Chernoby] nuclear
power plant accident etc., but the reasons are not yet
understood.
Recently, a pilot study was conducted that used
microarrays as one of the DNA studies related to genetic
effects of radiation. The microarray used consisted of
about 2,500 DNA clones (termed PAC or BAC) that were
selected among the huge number of clones prepared for
human genome project. The array could detect copy-num-
ber changes (CNV; deletion or duplication) of sufficient
length (>30 kb) in the genome. Among the 80 offspring
examined, 251 CNVs were detected but all of them were
inherited from either parent. No suspected case was found
that could have occurred newly following parental expo-
) HHROWENZS Genetic Effects
aanty LELENSILTNTHIKEB SRO
ICFFEL TREND CHOK. MORES EL CHE
as EVER BED ALA) PIL Pork. GRILLS ¢
DT) LEME LC ade % 17 9 ETC S ©
2212. REBR OLED I AGF IA bitte fHelc
BUTS PRB GE 81
Table 12. Mutations at minisatellite loci in children
of A-bomb survivors™
BM LV ARAB RB AE L ACB
ju-7 New fattationnenmetes examined
Probes <0.01 Gy 20.01 Gy*
XTM-18 0/183 0/65
ChdTC-15 0/183 0/65
Pags 0/183 1/65
AMS-1 11/183 1/65
CEB-1 11/183 4/65
Pc-1 0/183 0/65
B6.7 6/160 3/56
CEB-15 7/182 0/63
fat Total 35/1,440 9/509
(48 Frequency) (2.4%) (1.8%)
* BAP Uc -Fiitie 1.9 Gy
* Weighted mean dose 1.9 Gy
RCBEBKLUPA HERS 6
REA CL, LSS BANBS ABER OTHE,
5 Aae5 198446 12 ECILAHENEACOWT, SUZ
LODA AE & PRA LCS. CORMO Fiepls
2007 EOKERLC 23 HEADS 61 EO SEPA HY . PEt
ATI CHS. CME COMRMRICL SL, 20m GTS
Vd 20 RELAIS BIT A DAFA E LILWABEOT OF
FRICKE ARCO PMSA SNC, LAL
COPMICLBIVAREOILLEA FISGRBETS EM DIN
BOC, FREEZES BLO ETON ERO 52 (= BY
1946 4F
oe
=
ra
LC bait EE ¢ 72. SRE RW Oe AA
KECH So. F, RMI BW SMEARS — 7 RIA (LECH
Ko
sure to A-bomb radiation. Further studies are under
consideration.
#138. DNA 71 YA-TVY hICBIFSE RRB ©
Table 13. Mutations in DNA fingerprints®
<0.01 Gy 20.01 Gy
FED Bi
cinibless c a
HI LINY FORSBEL
Total bands examined a deal
BT LV ZEPR IE FRE 13 1
New mutations* (1.2%) (1.1%)
*Z EF MET O— 7 33.15 ic £0 RH
*Detected by a multilocus probe, 33.15
Mortality and Cancer Incidence in F,
Offspring®*©®
RERF is monitoring mortality and cancer incidence in
persons born between May 1946 and December 1984 to
LSS survivors. As of 2007, cohort members ranged in age
from 23 to 61, with a mean age of 47 years. To date, there
has been no evidence of increased cancer incidence or
increased mortality from cancer or other diseases either up
to age 20 or after age 20. Much longer follow-up is needed
to reach any conclusions regarding the effects of parental
A-bomb exposure on disease occurrence, since most of the
disease occurrence in this cohort is still in the future. Table
14 shows recent summaries of mortality data for this F,
cohort.
Genetic Effects KHROBGHRS i
2614. BHT OS MIC BUT SB AFM LUZ BABEORBALIOREICAF SE VF— FILE (20 weit E 20 LAKE) .
QTNOGHS. RANCHER EF— KROME SN TPZ.
Table 14. Adjusted hazard ratio for cancer and non-cancer mortality before and after 20 years of
age in F, offspring.™ No statistically significant increase in hazard ratio
has been observed for cancer or non-cancer mortality.
~SASCLE Cancer death DSALWSH-OXEE Non-cancer death
1-19 ink 20 ine DAK 1-19 ise 20 ink LAE
Age 1-19 years Age 20+ years Age 1-19 years Age 20+ years
BLAST L eta
Weighted dose LR FH FER Aoi We AOR FER Vor
(mGy) No. cases Hazard ratio No. cases Hazard ratio No.cases Hazard ratio No. cases Hazard ratio
RBLO ER
Paternal exposure
<5 (ASFaHE Control) 8 1.00 73 1.00 219 1.00 110 1.00
5-149 22 0.84 74 1.05 50 1.39
| 6 | 0.84
150-500+ 20 0.90 64 0.92 31 0.99
EE BLO BUR i
Maternal exposure
<5 (A}FaHE Control) 16 1.00 128 1.00 331 1.00 176 1.00
5-149 68 1.43 126 1.04 119 1.01
| 12 | 0.79
150-500+ 38 0.94 102 1.00 53 1.09
) #42 Radiation Dosimetry
HRS Radiation Dosimetry
ies hie tee 8 Physical Dose Estimates®*5
FAZER ICD A HEE aK Ik 2002 FE ICH A Ke The Dosimetry System 2002 (DSO2) provides individ-
4 (D802) C, #EERH A TEMPUS BIS 2 WRIC IES ual dose estimates based on information regarding each
a gine eps ’; tsye,- SUrvivor’s location and shielding situation ATB. This sys-
VCR 4 A ORI @ HERE TS So DSO2 IIA Re «FMI tem was introduced in 2002 and is based on the physical
(EFA SURED DBRS HC. BC S aU BUNRO HH nature of the bombs dropped on Hiroshima and Nagasaki
7p OIC PUR MDS Zee EO EF CHB. ESE A(K | and theoretical models developed by nuclear physicists for
DOMES HET SIC POLS EBBESVIEMICOWT the amount of radiation released, how this radiation was
transported through air, and how it was affected by passage
through physical structures and human tissue. These mod-
DCHS. DET WIL, KEOBU BA CHET Y 4 IV? ote were validated using measurements of existing exposed
LEE) OPER RIA EA MAED Ze SITS. Hl 191k, | materials, such as wall and roof tiles. Figure 19 shows air
Zerh wee (> 7p db, WERROZVMIRAE) £ELIMibg > OHH | doses (i.e., no shielding) according to distance from the
AEB ICT Li bOTCHS. BEOTD, MORE DS OR hypocenters and makes reference to corresponding biologi-
ieee _ cal effects and to comparable doses from other sources.
BETNICLSZEWMSN VE SAT o
DIZ EBA ED BERNE PV ICFEOVS CHAT SNES
19. BEDI 5 OFERE L ZB Rit & ORR. BREN CREA CBIR LEGA BHRBIZ 50% LEMD TS 0
AMIE RB CAEDFIIER, BEOCOMORH RUC EB RIB EAT
Figure 19. Relationship between distance from hypocenters and radiation dose in air. If inside a typical house,
the dose is reduced by 50% or more. Shown at the right are general biological symptoms and
radiation doses from other sources.
100
50rS. — [KS Hiroshima
SS ea Rllé Nagasaki REO RRL ko CéM APS BCARIAIC1 00% TS
10 a 100% death within several days to weeks with modern medical
Soe interventions
5s cS HVE
1 oe Gamma rays t got, mt&4 Vomiting, nausea
05 Bee tL SERB Decrease of lymphocyte counts
Ss BE FOBAD5S RR RIE COR DO B ARO &
Se Cumulative dose of residual radiation beyond the first day
hee NSN 1+ BOR (HRB)
Say Gastric fluoroscopy (skin dose)
zechipe (Gy)
Air dose (Gy)
ic
*S\\Neutrons
s.
+ FV WI7DOK (BR) RS
0.001 , e| Annual background dose
1 + BLY 7 ARR
500 1,000 1,500 2,000 2,500 Chest X-ray photography
IRL HDS © FEBE (m)
Distance from hypocenters (m)
FEA Ze PRIL, 1940 4E(R BEE 1950 4ECCHIAEIC LSS Basic shielding information is available from data
AIO ISIE (ot L CH DN MERRO PF [EO obtained through interviews conducted in the late 1940s
~ and early 1950s for nearly all LSS members. In the late
y . SpA EAE SP ACHIAE IZ fe
CIS a ES PDO ie tee TG Pe ESS ei 1950s and early 1960s more detailed shielding histories
OLEH OK ke CILEE LSA #9 1,600 m LIAL, FIRS Were obtained for nearly 85% of LSS survivors who were
(£2,000 m LIN MHI) OH 85% (COU C HICH EAE = proximally exposed (within 1,600 meters of the hypocen-
AMEN. CNOEOF—V¥ ICH, HA 10,000 m | ter in Hiroshima and 2,000 meters in Nagasaki). On the
DAPS-CHEBE L 72 LSS SEF 93,741 A. 5 86,671 A, (92%) Ic basis of these data, DSO2 dose estimates (Table 2 on page
Ceo: cae 7) have been computed for 86,671 of the 93,741 LSS
VST DS02 HEE BRE ASATSE SIU TW S (TR —- YD, HK2) | survivors (92%) who were within 10,000 meters of the
(2,000 m LAA CIE 84% ) 0 UHRA BEES VMSA ZIRE CH= hypocenters ATB (and 84% within 2,000 meters). DS02
WELT (ay 7 — EMA ORR &) 7,070 A Oiutiheeee | dose estimates could not be computed for the 7,070 proxi-
PRY (ZO VT lk DS02 HEGEBURO SMELL CR TEE mally exposed survivors with complex or unknown shield-
ing (e.g., exposed in a concrete building).
Radiation Dosimetry HARE fj
{a 2 Opt ee Mlk, A < OBIT NAR BRBSSL Individual dose estimates are imprecise for various rea-
DILMIEM REO DHS. AVC S SEMEL L__-- 8ONS, including inaccuracies in reported survivor locations
SIEM CEPR ORL, WRBICe CEO EF BUND 5
IGS UTWL PINT © FL CIT SC CILAATHET | technical issues regarding their radiation characteristics
and the impossibility of accounting in detail for all aspects
of shielding. In addition, the yields of the bombs and some
hokrtBhpns. BHicld, MRPoMMHSNeL*AW can only be estimated. Generally speaking, it is believed
3 DOHC OPE EIS BI S BOOM Ze RH BA la, He that standard errors in individual dose estimates may be on
WIS ALPE AV. HRATICIL, 1A AOE
AES PEARSE LW 35% C DEF ZENTWSA!, TILK
the order of 35%. Special statistical methods reduce the
Ait <
Tul
systematic effect on risk estimation arising from such
errors.
PRAEDS AT HEFE NK MES ARH HOE IM SES ED Most radiation exposure was from gamma rays with a
\ARBE e RESEDA ENTS small neutron component. In Nagasaki, the neutron compo-
EBUMOIEL Alby WELCH ORD, HELO RE nent appears to be virtually negligible. In Hiroshima, it is
LAN RS ‘) 77) WK re ay en
DOoPLFELK. COMMF ORG, RICE OK DTD
somewhat larger, up to a few percent of gamma dose for
shallow tissues at the most proximal distance where survi-
Choke Ikke Cltklliy £ Y Rar < . Heb WEEE CHELZ —-vors were located, but this ratio of neutron to gamma-ray
DV —S Die ERE CLT V VEE OBL% TERE CH 7 Fed8, | dose is lower for deeper tissues and falls off rapidly with
HY VOLES ZCOMUEF- OMSL, MBOPEMBIC ES UE distance (Figure 20). Neutrons are believed to have a
CMR EN EERE 5 OPTREIC AE IMR Le (1K
greater biological effect per unit dose than gamma rays.
Thus, many analyses use a weighted total dose in gray
20) 0 HEF IL Ay Vik EO} BUNGEE 29 OAR DENYS (Gy) units, which consists of neutron dose multiplied by
RIBREW. COC. HEF Hoe LOFT SHAT LT | ten plus gamma dose.
AY hee IM 7s
[hy
EDS ¢ OAT CHV 5SIVTWSo
20. ACERS GOR LS BBL SVC BITS DY CRI TB PEF MUO WG ©
WI SHEFREORMA (%)
Ratio of neutron to gamma-ray dose (%)
Figure 20. Neutron dose as percentage of y-ray dose for successive levels of
shielding and self-shielding®?
I & Fe ly
Hiroshima 10 Nagasaki
WT SPEFREOSIA (%)
Ratio of neutron to gamma-ray dose (%)
0.3 0.3
iy ug
= 5
9 0.1 bss 0.1
\ ‘
0.03 0.03
1,000 1,500 2,000 2,500 1,000 1,500 2,000 2,500
ei sthD 5 OD EBBE (m) ie tth D5 OD EBBE (m)
Ground distance (m) Ground distance (m)
Air dose* WIRE Shielded dose
Marrow dose —-—-—#éla#= Colon dose
“ROR LUIA OZ Re Air dose without shielding
) #42 Radiation Dosimetry
DS02 (2 ko 15 MAO EO WY VBL L AEF O hie
HEE CAA. CNS OMA IL, AED TERCIKULD 1S
Dic, BURFOMKO IA S PRA BML TABI L 4 likeat
DRUK D AICA NCS BAH ODS A & MATS S
& RIL Slee DAV SITS 6
Vv
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ee NIL. PERO HEIC SOO EBONVEM Flic
LS¢DICKWMSENS. POH CIS. ERIN TRA BL%
BEN TOPE, WHERIBTAC EI koTHE
US ROHED DEC. BRIMBIGIEVIE CHEBS Us, CINE
Clit SNE Cd, ERED 5 SH ICES E COR
WON Mes LED CRA 0.8 Gy URIS) B EU 0.3-0.4 Gy
(Rle}) EBRGSNTTWHIHS. ERED 5 O IRAEDS 500 m
PACED Hb lc BIT SHOR 1/10, 1,000 m Clk #9
Wl00 EBLRSENTWH. COBB HELE FARE
WAC FEI Le (M21). T#ebb, Hee 1 AA
Lit HOW 80%. 2-5 HAE CIM 10%. 6 HALA
(FE) LOWDMHSNLEBLZSNTIS. Hebd Els,
KEBORSBAECILEAEMBAY) CARMOKRCE
EAA L, PHONIC LA ithe lt, hace DIO
{HM 20% UK ES ClE 0.16 Gy, ElFCIL 0.06-0.08 Gy) %
WAZ EIMELALRPOKOCLAVPLEDNS.]
DLEIE DS86 Ic FEO < HEE CH 4S. DS02 (CHO < HEA Ze FT
FULTON CRRA, AEF ORC &b LAV AR
BVICSRULAHVNERO LO, MRE A ER CICK
SLEBRGNSA.Q
WUNTERE Flt, BE LCE OD FAVA SAW IE
FV RAD LORD RO RGR C7 HUNTED A ICHRS A ©
FRGHO KER & FEC HN ED Alt LA LGH SN, ZO—*
Fumi c eo CMO WEhETELE (BURO ER hor
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ab (EEF WIGENS HY VRBEDE b Borde -
AX SPE TIAN). RI CULES (PH LUHW IX) 1c
CEU COMERS EST Y VRAORKIMMBEE
MBL, bOLRHEZCICEEEDKRERELT. KBOD
22 + EAM Clk 0.01- 0.03 Gy, EMFO VENA Cle 0.2
—0.4Gy CHEE SNA. BeLHICBIT SMP ICES
PURPLE IL LILO MOM INO bCBASN WS. EK,
PWM O COARAICE AB L 7. ARSC TEES 2 Rp aT
OBE PRO CERI ETCH lc k SURO Hse os, PLL Hh
D-MOEREMRI CT bnk. SABMAEATH Re CIC E
ee eget ieee
pl
pal
Ix
DS02 provides estimates of gamma-ray and neutron
doses to 15 organs. These organ doses account for shield-
ing of the organs by the body and consider the survivor’s
orientation and position ATB as well as external shielding.
Analyses of cancer risks at specific tissue sites are based
on these organ doses.
Residual Radiation”*””
There are two types of residual radiation: induced
radioactivity and radioactive fallout. Induced radioactivity
results from the interaction of neutrons (a small component
of A-bomb radiation) with materials. Doses due to induced
radioactivity were highest at the hypocenters. Past investi-
gations have suggested that the maximum cumulative
doses of residual hypocenter radiation since the bombing
are 0.8 Gy in Hiroshima and 0.3 to 0.4 Gy in Nagasaki. At
500 and 1,000 meters from the hypocenters, the respective
estimates are about 1/10 and 1/100 of the hypocenter
value. The induced radioactivity decayed very quickly
with time (Figure 21). In fact, nearly 80% of the above
doses were released within a day, about 10% between days
2 and 5, and the remaining 10% from day 6 onward. Con-
sidering the extensive fires near the hypocenters that
prevented people from entering the cities until day 2, it
seems unlikely that any person received more than 20% of
the maximum induced doses (0.16 Gy in Hiroshima and
0.06 to 0.08 Gy in Nagasaki). All the calculations were
based on DS86. Detailed calculations have not been per-
formed for DS02, but would be very similar due to the
similar numbers and energy spectrum of neutrons.
Radioactive fallout primarily came from radioactive
atoms produced by nuclear fission of the uranium or pluto-
nium in the bombs. Radioactive material in the bomb fire-
ball ascended and cooled, a fraction falling as “black rain”
which contaminated the ground (although the black rain
was primarily soot particles from the extensive fires).
Because of wind directions, the rain fell mainly in northern
and western Hiroshima, with the highest measured gamma
dose rates from fallout being in the Koi-Takasu area to the
southwest, and in eastern Nagasaki, in the Nishiyama area.
The maximum estimates of fallout dose from external
exposure to gamma rays, assuming that a person remained
in one place throughout life, are 0.01 to 0.03 Gy in Koi-
Takasu, Hiroshima, and 0.2 to 0.4 Gy in Nishiyama,
Nagasaki. The corresponding fallout doses at the hypocen-
ters are believed to be only about 1/10 of these values. The
doses due to internal deposition of long-lived fallout radioi-
sotopes present in the environment, i.e., due to dietary
intake, were estimated for a sample of Nishiyama residents
based on measurements including whole body counting to
determine each person’s body content of a key radioiso-
tope, '37Cs_ and were found to be minimal.
Now, more than 60 years after the bombings, ultrasen-
Radiation Dosimetry HARE [fj
B21. REDAORL 1 m (CBT S PNP L BRIER O REET
Figure 21. Radiation dose at one meter above ground level at hypocenters, by time after detonation
15
1 minute
TREY KW ORY VERE (Gy)
Gamma-ray dose (Gy) per hr
1 BSTal
1 hour
1 fel | S=
1 week 1 year
148 |) Zaz
1 day |1 month
BRB RROD LAL
Background radiation level
10 10° 10° 10* 10°
I FE12 O Beef] (h)
Time after detonation (hours)
eatW LMA, HERES OK DTD CHOK.
60 ELLA REL BUE CIS. PSN TIE WIGET S 72 (o
LARGE Ze ER REO BPE CHS (Lb YRS
FEO CWDEMILIEAD DF PLARY). Ee. BUNVEM
PW DUE dBA CLE (1950 4E(KDS 1960 FARIS BUT
CHR CAT DN EK ART RIC ESIC KW SO
DHE LOBE Ch So JAR + RUMOR BUNS ES
tm (SBE. PHN FD Re EO ARB RIC LS
LAVEIS MIP Ho THOS (221). BONER Wb E
OFF BUN BE FE + BAIL Ove Clk, DS86 REO
6 Hla AN ee ADS 4% ©
sitive equipment is needed to measure induced radioactivi-
ty, and only a few exposed buildings remain in which it
can be measured. Measurement of radioactive fallout is dif-
ficult, and distinguishing the fallout caused by the bomb-
ings from that produced around the world by atmospheric
nuclear tests in the 1950s and 1960s is usually not possible.
Current annual doses from residual radiation in Hiroshima
and Nagasaki are far below levels of natural background
radiation from cosmic radiation, radon, etc. (Figure 21).
Chapter 6 of the DS86 Final Report provides an extensive
documentation of measurements and calculations related
to both fallout and induced activation.
§) #848 Radiation Dosimetry
yA GB ee o8
Mmigeh £k OPRAH A VAICIL, RERUN BLO BAERS
BEV AW Catgr STH. BUN ile OA AO ze Lc
AIT SCE ASMHECHS (Z 15).
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ede (Few 7s we) 7 Uefa fRIC4E Ue DNA OSE
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ACERI SLWVI RCA, CNECOLI ARBAB ICE
S4ZbOlk%V. AHS KA HORO TWA REED ye fh
(KE BVEIL, ARREBA CH LCN OFEe Re & PEEL
RARBED) b 30-40% KY CEA Pork. COIL,
Tai ABU D BLED HE TE RR se & GRAM SU BEDS H
SLLEMRBLTWIS.
oth
Biological Dosimetry’®
Some effects of A-bomb radiation are “recorded” at
molecular levels in blood cells and tooth enamel. As a
result, years after exposure, blood cells and teeth can be
useful for quantitative biological measurements of radia-
tion dose (Table 15).
Methods using blood cells measure DNA damage to
specific genes (mutated cells) or to chromosome structure
(chromosome aberrations). To date, chromosome aberra-
tions are the best long-term indicator of radiation dose.
Chromosome aberration frequencies for AHS factory
workers in Nagasaki have been found to be 30-40% lower
than those for survivors with the same estimated dose who
were exposed in houses. This difference suggests that
the current factory-worker dose estimates need to be re-
evaluated.
E15. NBER SHEET 4 720 DEWPT
Table 15. Biological methods for estimating radiation dose
Ti 2 mi Bh
Methods Materials
Y VINER BUS ERG
Chromosome aberrations in
lymphocytes
IfL#Z Blood 2 cc
TF fk
Characteristics
(sae Spapiling
Useful any time after exposure
Bi 2 IVE< BIT 4 ESR BA UE EIS
ESR in tooth enamel Extracted tooth Useful any time after exposure
Y YNERIZ BI S TCR RARER
TCR mutation in lymphocytes
PUR EAM b Ro CRO POMEF ICAL CHT ONE
PRBE SR) YIN ERAS CUS UU O BOE & PRI TSE
BCKRPOK. Bic, RARERISH MIC Lo COA
CZbOCLEVOTC, DNA BARE RUEEO AA MELB
bNTWS. RABRIL, MATRIC PRo TARICE LS
SNH), CNOORBMMIOMGIL, Fite ICH
Ly SOMEICILKA BIW AEDED5NS. COLIAR
TUL CL, Dae O BRUNO HAE HIS — © USARICHEL Vo
Ex, MAIL DNA GEIST HEADS OCS CIK
it CLG CHS. filo CT. GHOREL Ait ite EIT
Che ¢. RURORAE CSIC OA SND AER
DEO EERE DS, HIRE ASPEN E LIER) TAU
HO UN REE C > Th. RO EF (CBR IC PRER LZ
Grek, FrVIT 4 V BRROGRMIMIEDAD ED
CRM pkKoCPL FORM: LU SHEE CIS, Be
RIC SLU LEY BOD DHAKA Vo
PRD RX VAIS NK COD FV AVEWET ATE
IflL¥Z Blood 1 ec
RS < PUR eB ALA HT He
Possibly useful within a few months after
exposure
Various assays of lymphocyte gene mutations did not
detect A-bomb radiation effects when tested many years
after exposure. The usefulness of DNA mutation assays is
further limited because mutations are not caused by radia-
tion alone, but by a variety of other environmental toxi-
cants as well. Mutations also arise naturally when cells
divide, and their frequency increases with age and can vary
greatly from person to person. Under such circumstances,
the effects of low-dose radiation are particularly difficult
to detect. Cells are also able to repair certain kinds of DNA
damage, especially at low dose levels. The extent of dam-
age depends, therefore, not only on total radiation dose but
also on modality of exposure or dose rates (acute vs.
chronic exposure, single vs. fractionated or repeated dos-
es). The effects of acute single-dose exposures, as in the
case of the atomic bombings, are greater than the effects of
the same total dose received over a long period of time in
repeated or continuous low-dose exposures, as in the case
of people living in the area contaminated by the Chernobyl]
accident.
Measuring CO, chemical radicals in tooth enamel is
b, HADSIRAY VREORMMICAACHSZ. COW
Slick, TAR EOP CRP 5 Lt AW A HE
LC, BEA YIEIB (ESR) EW OAECI VA Vie Eilll
FEF Ao ESR OFS FOURS (LST HNO ILE BIS A
DOC, PORN P Pb St. WRAY te A abil & i
PET AC LACKA. COPE FovsT747F
Hitz CIS BU S REE O hee lc A SITS 0
Ye ARH OWI, BURR. RVMEA eR ICIS
PER PLA ERG ILHE LV. SORPRIL, MY 78
SRL PM 5S <6 ORME ER CEEN TSC 440%
OC, PRATT E LV 3 ERI DREAL CT LED 4, AS
LTWSAY YIANERD ED < SW ORADHRERLZEY VY 7NER
ROD (HOWL BBE Lea MIC RT Sb ORD
BD) DADS BWOBS CHA. I CURR ICOW THO
ESR F—¥Y EY YINSERO RRS TY EMA G DEN
IX. £0 TEWE eA Ae © EE CA SPSLNA
Vo
ait
Radiation Dosimetry HAGE
an effective assay for gamma radiation dose. Enamel is
separated from teeth that have been extracted for medical
reasons, and the presence of radicals is quantified by a
method called electron spin resonance (ESR). Because the
ESR signal intensity is linearly correlated with radiation
exposure, it can be used as a direct measure of physical
total dose, regardless of exposure modality. Presumably,
this method can be useful in assessing radiation doses in
situations like the Chernobyl accident.
Chromosome aberration data by themselves are not
enough to calculate radiation dose directly when years
have passed since exposure. This is because blood lympho-
cytes are produced through various steps from bone mar-
row stem cells, and it is unclear what fraction of the cells
examined are derived from irradiated lymphocytes (or
derived from irradiated bone marrow stem cells) when dec-
ades have passed since radiation exposure. Examination of
both tooth enamel ESR and chromosome aberration fre-
quency in blood lymphocytes from the same donors may
help us get better biological estimates of radiation dose.
43|
a ij a—7-— Frequently Asked Questions
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Frequently Asked Questions
Question 1. How many people died as a
result of the atomic bombings?**
Deaths caused by the atomic bombings include those
that occurred on the days of the bombings due to the over-
whelming force and heat of the blasts as well as later
deaths attributable to radiation exposure. The total number
of deaths is not known precisely because military person-
nel records in each city were destroyed; entire families per-
ished, leaving no one to report deaths; and unknown num-
bers of forced laborers were present in both cities.
The 1950 Japanese national census, carried out five
years after the bombings, provided a rough estimate of the
number of persons who were exposed and survived the
bombings. Approximately 280,000 persons indicated that
they had been “exposed” in Hiroshima or Nagasaki. The
so-called “early entrants,” who entered the cities after the
bombings, are not included.
In Hiroshima, an estimated 90,000 to 166,000 deaths
occurred within two to four months of the bombing in a
total population of 340,000 to 350,000. In Nagasaki, some
60,000 to 80,000 died in a population of 250,000 to
270,000.
Question 2. How many cancers in A-bomb
survivors are attributable to radiation?
Table 16 summarizes the number of cancers (from
1950 to 2000 for leukemia deaths and from 1958 to 1998
for solid cancer occurrence) in LSS A-bomb survivors in
relation to radiation dose. The proportion of cancer deaths
attributable to radiation exposure is considerably higher in
those exposed closer to the hypocenters (as is the case with
acute deaths from injuries and burns) (see also Tables 3
and 4). Overall, nearly half of leukemia deaths and about
10% of solid cancers are attributable to radiation exposure.
If one assumes that LSS survivors represent about half of
all survivors in the two cities, the total number of cancers
attributable to radiation exposure through 2000 may be
about 1,900 cases.
Table 17 presents the rough idea regarding the dis-
tance from the hypocenters and radiation dose.
Frequently Asked Questions #4] —7— B
#16. MAN OMA MAH CULE 5 OU HIE DS A FENE ATL
Table 16. Excess numbers of leukemia deaths and solid cancer occurrences in relation to dose
nlite sp 1eam [VAS A 58 9E
Leukemia deaths" Solid cancer occurrences’”
HANI LE WRK Alm Ween wSeele WRAR DATE Hen FSG
ie No. No. 92 Attributable No. No. 3% Attributable
Weighted subjects leukemia Estimated fraction subjects cancers Estimated fraction
dose* (Gy) excess (%) excess (%)
<0.005 7
HEE Control 37,407 92 0 0% 60,792 9,597 3 0%
0.005-0.1 30,387 69 4 6% 27,789 4,406 81 2%
0.1-1 16,108 all 34 48% 14,635 2,800 460 16%
21 25109 64 56 88% 2,210 645 307 48%
I REAS
BURRS aT 49,204 204 94 46% 44,635 7,851 848 11%
Exposed total
*AMROWALBANU Le Ahi CHEF Re LOR LR SDEAYVREOA). A
EIS A OMG lLBA LT
Wott. BAT AR DHA 5 OFPBElCOVe TlL# IT EB.
*Weighted bone marrow dose (10 X neutron dose plus gamma-ray dose) for leukemia and weighted colon dose for
solid cancers. For indication of the corresponding distance, please see Table 17.
TH AAN tee (NIC) #ISIBASAICILE EN THAD,
Al OIA GISELE EM TW RV
**These include not-in-city (NIC) group, which is not included in the leukemia data.
#17. LSS HRAODBRALS U7 HUB FIR EE DID 6 OFLHEO PIR. U
MANIC E 2 CHERUB BAEDC. oOphit Ee AHED PIGS
WELZ CB FET 24 TILE SHU TlEBUO.W
Table 17. Mean weighted colon dose of LSS subjects and the corre-
sponding distance from the hypocenter." Since shielding
conditions differ among the survivors, this radiation
dose-distance relation does not apply to everyone.
BARU Loti
Bebb 6 OB Ee OPE
Approximate distance from hypocenters
Weighted colon dose JA%§ Hiroshima fell} Nagasaki
0.005 Gy 2,500 m 2,700 m
0.05 Gy 1,900 m 2,050 m
0.1 Gy 1,700 m 1,850 m
0.5 Gy 1,250 m 1,450 m
1 Gy 1,100 m 1,250 m
BS MHP RA CEAZSHNSPAISS
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Question 3. Are radiation-induced cancers
still occurring?
Cancers attributable to radiation are still occurring
among A-bomb survivors. The excess risk of leukemia,
seen especially among those exposed as children, was high-
est during the first ten years after exposure, but has
decreased over time and has now virtually disappeared. In
contrast, excess risk for cancers other than leukemia (solid
cancers) has stayed constant and seems likely to persist
throughout the lifetime of the survivors.
a ij a—7-— Frequently Asked Questions
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Question 4. What radiation effects have
been observed in people exposed in utero?
Many health effects are associated with radiation expo-
sure before birth. Effects noted among A-bomb survivors
exposed in utero include a reduction in IQ with increased
radiation dose, a higher incidence of mental retardation in
those heavily exposed, and impairment in physical growth
and development. Many of these effects seem particularly
pronounced in persons exposed between weeks 8 and 15
of gestation. Death rates and cancer incidence are being
monitored for this group. Previous data suggested a dose-
related increase in cancer risk similar to that seen in A-
bomb survivors exposed as children, but more recent data
indicate that the risk is lower in the survivors exposed in
utero (page 28).
Question 5. What have been the genetic
effects of radiation exposure?
One of the earliest concerns in the aftermath of the
atomic bombings was how radiation might affect the chil-
dren of survivors. Efforts to detect genetic effects began in
the late 1940s and continue. Thus far, no evidence of
increased genetic effects has been found. This does not
necessarily mean that no effects exist because some past
studies were limited in their ability to detect genetic dam-
age. Recent advances in molecular biology make it possi-
ble to evaluate genetic effects at the gene (DNA) level.
RERF scientists are preserving blood samples that can be
used for such studies. Monitoring of deaths and cancer inci-
dence in the children of survivors continues, and a clinical
health survey was undertaken for the first time during
2002 to 2006 to evaluate potential effects of parental radia-
tion exposure on late-onset lifestyle diseases. To date,
there is no radiation-related excess of disease in adulthood,
but it will require several more decades to fully determine
this, as this population is still relatively young.
Question 6. Who make up the RERF study
population?
To establish a population framework in which to con-
duct long-term follow-up of mortality and cancer inci-
dence, about 94,000 people were selected from 280,000
A-bomb survivors who were resident in Hiroshima or
Nagasaki at the time of the October 1950 Japanese
national census. Of these, about 54,000 were exposed to
significant radiation doses within about 2,500 meters from
the hypocenters. Another 40,000 members of the study
population were exposed beyond 2,500 meters and
received very low doses. An additional 27,000 who were
not in Hiroshima or Nagasaki at the time of the bombs, but
whose family registries were in Hiroshima or Nagasaki
and who lived in either city at the time of the 1950 census
also were included as an unexposed comparison group.
These groups constitute the 120,000-member LSS cohort.
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Frequently Asked Questions fi] —7— |
In addition to studying the LSS cohort, RERF scien-
tists are involved in studies of several other populations:
the AHS, in utero-exposed, and F, cohorts. The AHS popu-
lation comprises 23,000 members of the LSS, who, since
1958, have been asked to participate in biennial medical
examinations carried out at RERF. The in utero-exposed
cohort is a group of about 3,600 people who were exposed
to the bomb while in the womb. The F, population consists
of about 77,000 people born in Hiroshima or Nagasaki
between | May 1946 and the end of 1958 to parents with
and without exposure to the bombs.
Question 7. What percentage of A-bomb
survivors are included in RERF studies?
In the 1950 Japanese national census, approximately
280,000 people indicated that they had been exposed to the
atomic bombs. RERF’s study population probably
includes about 50% of those proximally exposed (within
about 2,500 meters of the hypocenters) and 25% of those
distally exposed (greater than 2,500 meters from the hypo-
centers). These percentages are not precise because the
census did not record the location of exposure in reference
to the hypocenters.
Question 8. What percentage of A-bomb
survivors within the study populations have
died?
As of 2007, about 60% of original RERF study partici-
pants were dead, but about 10% of those exposed under
age 10. Projections suggest that in 2020 those percentages
will be about 90% and 60%, respectively.
Question 9. What is meant by “significant
dose” when referring to radiation exposure?
In the discussion of cancer risks presented in this book-
let, attention is focused on survivors with estimated expo-
sure doses greater than 0.005 Gy (5 mGy). No excess risks
of cancer or other diseases have been seen among survi-
vors with doses below 0.005 Gy. A dose of 0.005 Gy is
somewhat greater than the typical annual background
radiation level to which people are exposed in normal daily
life (0.001 to 0.003 Sv per year, including radon) and
about one-fourth the currently accepted maximum annual
dose allowed for radiation workers (0.02 Gy). Survivors
with doses of 0.005 Gy or more were typically within
about 2,500 meters of the hypocenter in Hiroshima and
2,700 meters in Nagasaki. The average dose received by
such survivors is about 0.2 Gy. The radiation dose
decreased by half for every 200-meter increase in distance
from the hypocenters.
a iii a—7-— Frequently Asked Questions
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Question 10. How long were Hiroshima and
Nagasaki radioactive after the bombings?
Doses from residual radioactivity in both cities are
now far below the annual background dose (0.001—0.003
Sv); hence, there are no detectable effects on human
health. Radioactivity was over 90% gone by one week
after the bombings and was less than the background level
by one year (Figure 21).
There are two ways radioactivity is produced from an
atomic blast. The first is from the fallout of fission prod-
ucts or nuclear material itself (uranium or plutonium) that
then contaminates the ground, like the contamination that
occurred as a consequence of the Chernobyl accident. The
Hiroshima and Nagasaki bombs exploded 500 to 600
meters above the ground, and the explosions created huge
fireballs that rose with ascending air currents. The material
then cooled and started to fall with rain. Because of the
wind, the rain did not fall directly on the hypocenters but
rather in northwestern Hiroshima, in the Koi-Takasu area,
and in eastern Nagasaki, in the Nishiyama area. Now, the
radioactivity is so miniscule that it is difficult to distin-
guish it from background radiation or the trace amounts of
radioactivity caused by atmospheric nuclear weapon
testing.
The second way radioactivity is produced is by neu-
tron irradiation of soil or buildings. (Neutrons comprised
10% or less of A-bomb radiation. Nonradioactive materi-
als become radioactive after absorbing neutrons. In con-
trast, gamma rays, which comprise the majority of A-bomb
radiation, do not induce radioactivity.) Most of this
induced radioactivity decays very quickly, so that now it is
infinitesimal.
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Collaborative Programs HMMAARFOFTL I
Collaborative Programs
Japan Domestic and Japan-US Collaborations
RERF conducts collaborative research projects with
physicians and scientists from other medical and research
institutes, universities, and hospitals to expand our
research fields and strengthen findings on A-bomb survi-
vors. RERF is currently involved with the local tumor reg-
istries managed by Hiroshima city and Nagasaki prefec-
ture; site-specific cancer studies that include pathological
case review by external pathologists; and a variety of
specific collaborative projects with local universities.
We have an ongoing consortium with the University of
Washington and Kurume University that is conducting a
series of epidemiological and statistical studies of A-bomb
radiation effects. For many years we have had a collabora-
tive contract with the US National Cancer Institute (NCD
to conduct a number of epidemiological studies that have
resulted in many publications about radiation effects.
International Collaborations and Information
Dissemination
The results of studies conducted at RERF are analyzed
and disseminated throughout the world. Collected data elu-
cidate the effects of radiation exposure on humans and are
applied in establishing international radiation protection
standards. RERF researchers interpret study findings in
cooperation with the International Commission on Radio-
logical Protection (ICRP), the United Nations Scientific
Committee on the Effects of Atomic Radiation (UNSCEAR),
the US National Council on Radiation Protection and
Measurements (NCRP), and the NAS Advisory Commit-
tee on the Biological Effects of Ionizing Radiation (BEIR).
Members of RERF serve on several of these committees to
evaluate and provide timely information on radiation risks.
Following the Chernobyl accident in 1986, RERF has
become more directly involved in studies of radiation
effects in other populations whose exposures markedly dif-
fer from the exposures of atomic-bomb survivors. These
efforts have included collaborations with the World Health
Organization (WHO), the International Atomic Energy
Agency (IAEA), and Gesellschaft fiir Strahlung Forschung
(GSF) to evaluate the effects of prolonged radiation
exposure.
In a similar effort, RERF provided direct support,
under contract with NCI from 1995 through 2004, for
efforts to strengthen epidemiologic studies of workers and
members of the general public exposed to radiation as a
consequence of plutonium production in the southern
Urals of the Russian Federation. RERF also collaborated
with Russian research institutes, under contract with the
US Department of Energy from 2001 through 2005, for
development of a unified database to facilitate and
i HAT OTF L Collaborative Programs
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strengthen health effect and dosimetry studies on the Ozy-
orsk populations. Furthermore, collaboration with the
Kazakh Medical and Environmental Research Institute in
Semipalatinsk began in 2004, with support from the
Japanese Ministry of Education, Culture, Sports, Science
and Technology, for construction of a database for health
effects study of those exposed to low-dose radiation from
nuclear tests in Semipalatinsk, Republic of Kazakhstan.
In addition, RERF cooperates with two local organiza-
tions in Hiroshima and Nagasaki, the Hiroshima Interna-
tional Council for Health Care of the Radiation-exposed
(HICARE) and the Nagasaki Association for Hibakushas’
Medical Care (NASHIM). The two groups provide advi-
sory medical and technical personnel to countries where
major radiation accidents have occurred and funding for
staff from these countries to receive specialized training in
Japan, with RERF accepting several long-term trainees
each year, mainly from the former Soviet Union.
RERF welcomes trainees and visitors from around the
world, including researchers from the [AEA and United
Nations-related agencies. The World Health Organization
has designated RERF as a WHO Collaborating Center for
Radiation Effects on Humans since 1979 and a member of
the WHO Radiation Emergency Medical Preparedness and
Assistance Network (REMPAN) since 1988.
RERF Publications, Use of RERF Data RAHM. HBP 5 OSTA I
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RERF Publications and How to Acquire
Them
RERF Reports, which are reprints of papers published
in peer-reviewed scientific journals, have replaced RERF’s
in-house Technical Report series, which ceased production
in 1993. Manuscripts that become RERF Reports are first
approved by the RERF chairman following in-house
review before journal submission. After publication,
REREF purchases journal-article reprints, binds them into
RERF Report covers with Japanese summaries, and sends
them to interested governmental ministries and agencies,
local hospitals, libraries, and RERF directors and consult-
ants. Major reports are translated in full into Japanese.
The latest RERF news and research results are also
made available to Japanese and overseas research scientists
and the public via RERF Update, a newsletter aimed mainly
at a scientific audience; Commentary and Review Series;
RERF Annual Report; A Brief Description, a brochure con-
taining detailed explanations of RERF studies; Introduction
to the Radiation Effects Research Foundation and Basic
Guide to Radiation and Health Sciences for general visitors;
and RERF’s worldwide web homepage (http://www.rerf.jp),
where the latest bibliography of journal publications and
the abstracts of the ABCC-RERF Technical Reports and
RERF Reports are available.
The Public Relations and Publications Office, Secre-
tariat, is engaged in the editing and production of these
publications and in managing RERF’s homepage. To
request additional copies or further information, please
contact the Archives Unit, Library and Archives Section,
Information Technology Department. Request for RERF
publications can also be made through RERF’s homepage.
Fax from outside Japan: 81-82-261-3197
Fax from inside Japan: 082-261-3197
Use of RERF Data by Outside
Investigators
Procedures are in place at RERF by which outside
research investigators can have access to the data resources
maintained by the Foundation. Of prime concern is the per-
sonal privacy of data regarding individual A-bomb survi-
vors. Application for data access can be made to the RERF
Chief of Research, and stipulated procedures are necessary
for obtaining approval. Statistical, clinical, and epidemiol-
ogical data, masked sufficiently to prevent any possibility
of personal survivor identification, can be provided
through established RERF administrative procedures once
data collection, verification, processing, and primary in-
house analyses are complete. Access to individual survivor
data and biological specimens is possible in close collabo-
ration with RERF scientists and after full review by the
Wh RAL, 588% 5 ONMHFIAA RERF Publications, Use of RERF Data
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RERF Human Investigation Committee.
In addition, outside researchers can download from the
RERF homepage several datasets used for major study
reports, such as the Life Span Study reports. These data are
provided in such form that individuals cannot be identi-
fied, and all personal information is strictly managed by
RERF.
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Glossary BH OME I
Glossary
Physical Dose
One gray (Gy, 1 Gy = 1,000 mGy) represents one
joule absorption per kilogram of a given material. One
gray is equal to 100 rad (rad, 100 erg per gram, is a former
unit of dose). We receive 0.01 mGy (mSv) from ordinary
chest radiography, 3 mGy (mSv) from mammography, and
10—20 mGy (mSv) from abdominal CT examination, while
the dose received from the background radiation is 2 to 3
mSv per year (see below for Sv).
Equivalent Dose
Equivalent dose stands for a hypothetical dose that
takes into account exposure of different types of radiation
with different biological effectiveness and is expressed in
sieverts (Sv).
The majority of A-bomb radiation consisted of gamma
rays with a small fraction (less than a few percent of total
dose) of neutrons. Because neutrons affect living tissue
more strongly than gamma rays per unit dose, we therefore
use “equivalent dose” which is the sum of the neutron dose
multiplied by 10 (as a weighting factor reflecting its
greater strength) and the gamma-ray dose. Equivalent dose
is useful to express a more biologically meaningful dose.
At RERF, we formerly expressed these weighted doses in
Sv units. However, in the current practice in radiation
protection, the Sv unit is reserved for expressing average
doses that incorporate tissue sensitivity factors. Thus,
RERF decided recently to replace Sv with “weighted Gy”
to express equivalent doses and thereby avoid confusion.
Significant Exposure
In this booklet, “significant exposure” refers to doses
of 0.005 Gy or above, even though no excess risks of can-
cer or other diseases may be detectable at the low end of
this range.
Relative Risk (RR)
Relative risk is the ratio of the risk in an exposed group
to that in a comparable unexposed group. A relative risk of
one implies that exposure has no effect on risk. For
instance, the relative risk of leukemia is the largest among
various late effects; RR is about 5 or 6 per Gy (Tables 4
and 16).
Absolute Risk (AR)
Absolute risk represents the total number of persons
with a specific disease affected by radiation exposure, or
the rate of that disease in a given population over a given
period of time (usually designated as “person-years”). AR
is often expressed as the number of affected subjects per
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10* person-years or 10‘ person-year-Gy (i.e., per 10*
person-years per Gy). Whereas RR expresses degree of
excess risk, or strength of causation, AR describes the num-
bers of people affected and hence the public health impact
in a population. For instance, the RR for leukemia is the
highest among various late effects of radiation (RR
approximately 5-6), but the total number of radiation-
caused cases of leukemia in LSS survivors is estimated to
be only about 90-100 (Table 16). In contrast, the RR for
solid cancers is much smaller (RR approximately 1.5), yet
the total number of survivors who have developed such
cancers due to bomb radiation is estimated to be about 850
(Table 16).
Excess Relative Risk (ERR)
Excess relative risk is expressed as RR minus one, or
that portion of the RR accounted for by the particular risk
factor under study (A-bomb radiation, in this instance).
Excess Absolute Risk (EAR)
Excess absolute risk is expressed as the difference in
AR between exposed and control populations.
Attributable Risk
Attributable risk refers to the fraction of diseases or
deaths that is estimated to result from exposure to radia-
tion. It increases with dose. Total attributable risk for
leukemia deaths is nearly 50% and for solid cancers about
10% among LSS survivors who received 0.005 Gy or more
(significant dose).
Prevalence versus Incidence
Prevalence refers to the rate of patients who have been
diagnosed with a disease or medical condition at a given
point in time, regardless of when the diagnosis was first
made. Incidence refers to the rate of patients newly diag-
nosed in a given time period (usually one year), whether or
not they may have died during that time.
Hypocenter
The location on the ground vertically below the bomb
air-burst point.
Proximally Exposed
This term originally referred to persons exposed to the
atomic bombings within 2,000 meters of the hypocenters.
However, more recent RERF publications use the term to
refer to survivors who have estimated doses of 0.005 Gy or
above, which approximately corresponds to persons
exposed within 2,500 meters of the hypocenter in
Hiroshima and 2,700 meters in Nagasaki.
a Be RS
KES CIE Dab 5S 2.5-10 km OFERC. ECS
HbA 5 2.7-10 km Osi CHEE Le, 4
0.005 Gy Ait} ON FET
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Glossary BH OME I
Distally Exposed
This term refers to persons exposed to the bombings at
distances of 2,500 to 10,000 meters of the hypocenter in
Hiroshima and 2,700 to 10,000 meters in Nagasaki. Their
estimated radiation doses are less than 0.005 Gy.
a RIC Abbreviations
RIC Abbreviations
ABCC Atomic Bomb Casualty Commission JRE 5H HZ BS
A-bomb atomic bomb Jsi--ssl#
AHS Adult Health Study bk ) (#5 a2
AR absolute risk #fix}) A 7
ATB at the time of the bombing(s) #£28IRF (Age ATB : #K ERIE ZEN)
BEIR Advisory Committee on the Biological Effects of Ionizing Radiation #2 BERUN MELO EWA Wye 28 ICED S % ae
REA
RAR
CO, carbon dioxide =PR(biEX
DNA deoxyribonucleic acid 74 + KYM
DS02 Dosimetry System 2002 2002 4F-ii sete 7 Fst
DS86 Dosimetry System 1986 1986 4Fittarde ze 77 xt
EAR excess absolute risk 19) fax} 1) AZ
ERR excess relative risk #4#I4H%t AZ
ESR electron spin resonance Ef AE Y HIB
F, first filial generation #-fkOs3—tHt{t (ie., the children of A-bomb survivors : #R OF ft)
FISH fluorescence in situ hybridization (a technology to visualize chromosomes) #36 in situ?\7 TU Y4B@-Yav
(Bete th & wikia F 4 Bae)
GPA glycophorin A gene 7) A740 Y Aleta
Gy gray 7%
HICARE Hiroshima International Council for Health Care of the Radiation-exposed JCP EE ET IR EIS ih FFE ME
hie
IAEA International Atomic Energy Agency EMS 7483
ICRP International Commission on Radiological Protection uae maeARS
Kerma kinetic energy released in materials 7—Y WB IHH S 7c a EHV FE
LDsp 50% lethal dose 50% BOE HLRE
LSS Life Span Study Farid #
NAS US National Academy of Sciences *EI4#E/5é
NASHIM Nagasaki Association for Hibakushas’ Medical Care Ell} - EAT YD ~ RRA
NCI US National Cancer Institute 7<EIEIZ28 Ath
NCRP US National Council on Radiation Protection and Measurements *KEVPU EH - WIFERR BER
REMPAN WHO Radiation Emergency Medical Preparedness and Assistance Network WHO }iCp RSA NY
iS RHR AY hI 7
RERF Radiation Effects Research Foundation BOW BUNCE OCT
RR relative risk *1X}) AZ
Sv sievertt “~—“JU}
T65D Tentative 1965 Dosimetry 1965 422i 7E fst
TCR T-cell receptor T #H@ Ye TY —
UNSCEAR United Nations Scientific Committee on the Effects of Atomic Radiation EPR AA RUN a EES
BA
BAB
US United States 7 % ) 7 G3RE]
WHO World Health Organization THI MERE)
MPO RFICOUT
ks RMAs, EIROPLA PRY C. AEA D>
5 BEA E CO/F AI 9 RD 6 Fhe SRE CL MACS BIR
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CHhHEC KS. HL < ISR AN
wwwrrerf.jp) %# CHES RSV.
YD (http://
BB:
T 732-0815 JA eT rs X Sta Akal 5-2
BUNA TSCA
WG : 082-261-3131 (4¢¥)
77 VDA : 082-263-7279
Fel}
T 850-0013 Rll HII—T A 8-6
BUN LAE TSCA
#iah : 095-823-1121 (*t#e)
7777 RA 2 095-825-7202
RERF Tours and Further Information FLE#HO BAIS OUYT |
REREF Tours and Further Information
Our Hiroshima and Nagasaki facilities are open for
tours by individuals or groups Monday through Friday
from 9:00 to 17:00, excluding national holidays. For a res-
ervation of guided tour, please contact the Public Relations
and Publications Office, Hiroshima, or the General Affairs
Section, Nagasaki.
In addition, you may write, fax, or use the inquiry
forms on RERF’s homepage with questions concerning the
atomic bombings. For details, please visit our homepage:
http://www. rerf.jp.
Hiroshima:
Radiation Effects Research Foundation
5-2 Hijiyama Park, Minami-ku, Hiroshima 732-0815
Phone from outside Japan: 81(country code)-82-261-
3131 (Switchboard) (from inside Japan, use area
code 082)
Fax from outside Japan: 81(country code)-82-263-
7279 (from inside Japan, use area code 082)
Nagasaki:
Radiation Effects Research Foundation
8-6 Nakagawa 1-chome, Nagasaki 850-0013
Phone from outside Japan: 81(country code)-95-823-
1121 (Switchboard) (from inside Japan, use area
code 095)
Fax from outside Japan: 81(country code)-95-825-
7202 (from inside Japan, use area code 095)
i) S25: References
BZ Mk References
SMBH RE Acute Radiation Syndrome
1. http://orise.orau.gov/reacts/index.htm
2. Stram DO, Mizuno S: Analysis of the DS86 atomic-bomb radiation dosimetry using data on severe epilation. Radia-
tion Research 1989; 117:93-113.
3. HORA. Set, FE ae : BORER EE. AMEE 5 1995.
SE5EC Acute Death
4. Fujita S, Kato H, Schull WJ: The LD;, associated with exposure to the atomic bombing of Hiroshima and Nagasaki.
Journal of Radiation Research (Tokyo) 1991; 32(Suppl):154-61. (A review of 45 years’ study of Hiroshima and
Nagasaki atomic-bomb survivors)
BARBANK (7kgk14i2)H) Radiation Cataract (Lens Opacity)
5. Otake M, Schull WJ: Radiation-related posterior lenticular opacities in Hiroshima and Nagasaki atomic-bomb survi-
vors based on the T65DR and DS86 dosimetry system. Radiation Research 1990; 121:3-13.
6. Minamoto A, Taniguchi H, et al.: Cataract in atomic bomb survivors. International Journal of Radiation Biology 2004;
80:339-45.
7. Nakashima E, Neriishi K, Minamoto A: A reanalysis of atomic-bomb cataract data, 2000-2002: A threshold analysis.
Health Physics 2006; 90:154—60.
8. Neriishi K, Nakashima E, Minamoto A, Fujiwara S, Akahoshi M, Mishima HK, Kitaoka T, Shore R: Postoperative
cataract cases among atomic bomb survivors: Radiation dose response and threshold. Radiation Research 2007;
168:404-8.
EliZ+5A. Solid Cancers
9. Preston DL, Shimizu Y, et al.: Studies of mortality of atomic bomb survivors. Report 13. Solid cancer and noncancer
disease mortality: 1950-1997. Radiation. Research 2003; 160:381—407.
10. Preston DL, Ron E, et al.: Solid cancer incidence in atomic bomb survivors: 1958-1998. Radiation Research 2007;
168:1-64.
11. Preston DL, Pierce DA, et al.: Effect of recent changes in atomic bomb survivor dosimetry on cancer mortality risk
estimates. Radiation Research 2004; 162:377-89.
12. DVRTEIR, WKAR SS EERE BU RR IR GG TIE EL ho UTR O WME 1992.
MICH + 1992, pp 23-104.
13. Ron E, Preston DL, et al.: Cancer incidence in atomic-bomb survivors. Part IV: Comparison of cancer incidence and
mortality. Radiation Research 1994; 137:98-112.
Ail Leukemia
(SCHR 11 % BHR. See also reference 11.)
14. Preston DL, Kusumi S, et al.: Cancer incidence in atomic-bomb survivors. Part III: Leukemia, lymphoma, and multi-
ple myeloma, 1950-1987. Radiation Research 1994; 137:S68-97.
15. Bavillsr2. ACERMN. GREET 5S: ITI CRORE PR IR EL ah I HEHE Lah ho ER BUN TRO Ab
1992, MERE ; 1992, pp 35-47.
RMI Benign Tumors
16. Imaizumi M, Usa T, et al.: Radiation dose-response relationship for thyroid nodules and autoimmune thyroid diseases
in Hiroshima and Nagasaki atomic bomb survivors 55-58 years after radiation exposure. JAMA 2006; 295:1011-—22.
17. Yamada M, Wong FL, et al.: Noncancer disease incidence in atomic bombs survivors, 1958-1998. Radiation Research
2004; 161:622-32.
18. Inai K, Shimizu Y, et al.: A pathology study of malignant and benign ovarian tumors among atomic-bomb survivors—
19.
20.
21.
References SSX ff
case series report. Journal of Radiation Research (Tokyo) 2006; 47:49-S9.
Fujiwara S, Sposto R, et al.: Hyperparathyroidism among atomic-bomb survivors in Hiroshima. Radiation Research
1992; 130:372-8.
Ron E, Wong FL, Mabuchi K: Incidence of benign gastrointestinal tumors among atomic-bomb survivors. American
Journal of Epidemiology 1995; 142:68—75.
Kawamura S, Kasagi F, et al.: Prevalence of uterine myoma detected by ultrasound examination in the atomic bomb
survivors. Radiation Research 1997; 147:753-8.
BASS} ORRICK SFIEL Non-cancer Disease Mortality
CHK O & 17 % BHR. See references 9 and 17.
4ef4{42 Chromosome Aberrations
22.
23.
24.
25.
26.
27.
Nakano M, Kodama Y, et al.: Detection of stable chromosome aberrations by FISH in A-bomb survivors: Comparison
with previous solid Giemsa staining data on the same 230 individuals. International Journal of Radiation Biology
2001; 77:971-7.
Kodama Y, Pawel D, et al.: Stable chromosome aberrations in atomic bomb survivors: Results from 25 years of inves-
tigation. Radiation Research 2001; 156:337—-46.
BaP BESS: AAI SERDAR ERTS 0 BATT GRIER i I HE Ee 0 UIT IR O A
1992, MIE > 1992, pp 220-30.
Ohtaki K, Kodama Y, et al.: Human fetuses do not register chromosome damage inflicted by radiation exposure in
lymphoid precursor cells except for a small but significant effect at low doses. Radiation Research 2004; 161:373-9.
Nakano M, Kodama Y, et al.: Chromosome aberrations do not persist in the lymphocytes or bone marrow cells of mice
irradiated in utero or soon after birth. Radiation Research 2007; 167:693-702.
Kodama Y, Ohtaki K, et al.: Clonally expanded T-cell populations in atomic bomb survivors do not show excess levels
of chromosome instability. Radiation Research 2005; 164:618-26.
(AMAA E Somatic Cell Mutations
28.
29.
30.
31.
Kyoizumi S, Akiyama M, et al.: Somatic cell mutations at the glycophorin A locus in erythrocytes of atomic bomb
survivors: Implications for radiation carcinogenesis. Radiation Research 1996; 146:43-52.
Kyoizumi S, Kusunoki Y, et al.: Individual variation of somatic gene mutability in relation to cancer susceptibility:
Prospective study on erythrocyte glycophorin A gene mutations of atomic bomb survivors. Cancer Research 2005;
65:5462-9.
Hirai Y, Kusunoki Y, et al.: Mutant frequency at the HPRT locus in peripheral blood T-lymphocytes of atomic-bomb
survivors. Mutation Research 1995; 329:183-6.
Jensen RH, Langlois RG, Bigbee WL, et al.: Elevated frequency of glycophorin A mutations in erythrocytes from
Chernobyl accident victims. Radiation Research 1995; 141:129-35.
$2 Immunity
32.
33.
34.
35.
36.
Kusunoki Y, Kyoizumi S, et al.: Decreased proportion of CD4 T cells in the blood of atomic bomb survivors with
myocardial infarction. Radiation Research 1999; 152:539-43.
Yamaoka M, Kusunoki Y, et al.: Decreases in percentages of naive CD4 and CD8 T cells and increases in percentages
of memory CD8 T cell subsets in the peripheral blood lymphocyte populations of A-bomb survivors. Radiation
Research 2004; 161:290-8.
Kusunoki Y, Yamaoka M, et al.: T cells of atomic bomb survivors respond poorly to stimulation by staphylococcus
aureus toxins in vitro: Does this stem from their peripheral lymphocyte populations having a diminished naive CD4 T-
cell content? Radiation Research 2002; 158:715-24.
Hayashi T, Morishita Y, et al.: Long-term effects of radiation dose on inflammatory markers in atomic bomb survi-
vors. American Journal of Medicine 2005; 118:83-6.
Kusunoki Y, Hayashi T: Long-lasting alterations of the immune system by ionizing radiation exposure: Implications
i) S25: References
37.
for disease development among atomic bomb survivors. International Journal of Radiation Biology 2008; 84:1-14.
Fujiwara S, Sharp GB, et al.: Prevalence of hepatitis B virus infection among atomic bomb survivors. Radiation
Research 2003; 159:780-6.
Rt - 3 Physical Growth and Development
38. Nakashima E, Fujiwara S, et al.: Effect of radiation dose on the height of atomic bomb survivors: A longitudinal study.
Radiation Research 2002; 158:346—-51.
39. Nakashima E, Carter RL, et al.: Height reduction among prenatally exposed atomic-bomb survivors: A longitudinal
study of growth. Health Physics 1995; 68:766-72.
40. HAS Fh. PALA: BE CEA ORE BRIERE ER ES Tih HEE ES ho RIO 1B
1992. MIG ; 1992, pp 276-82.
Z1é Aging
41. Sasaki H, Wong FL, et al.: The effects of aging and radiation exposure on blood pressure levels of atomic bomb sur-
vivors. Journal of Clinical Epideiology 2002; 55:974-81.
42. Yamada M, Naito K, et al.: Prevalence of atherosclerosis in relation to atomic bomb radiation exposure: An RERF
Adult Health Study. International Journal of Radiation Biology 2005; 81:821-6.
43. Sasaki H, Kodama K, Yamada M: Aging. Journal of Radiation Research (Tokyo) 1991; 32(Suppl):310-26. (A review
of 45 years’ study of Hiroshima and Nagasaki atomic-bomb survivors)
44. Sasaki H: Aging. Shigematsu I, Ito C, et al., eds. Effects of A-bomb Radiation on the Human Body. Chur, Switzerland:
Harwood Academic Publishers; 1995, pp 316-23.
45. We AGE * DMT BITRE Ar RR a I HEHE La ES to ER CIRO WAREZ 1992. MIEHE + 1992,
pp 284-91.
RaA tte / tai ¢ KEES In Utero Exposure/Mental Retardation and Growth Impair-
ment
46. Nakashima E: Relationship of five anthropometric measurements at age 18 to radiation dose among atomic-bomb sur-
vivors exposed in utero. Radiation Research 1994, 138:121-6.
47. Otake M, Schull WJ, Yoshimaru H: Brain damage among the prenatally exposed. Journal of Radiation Research
(Tokyo) 1991; 32(Suppl):249--64. (A review of 45 years’ study of Hiroshima and Nagasaki atomic-bomb survivors)
48. Otake M, Yoshimaru H, Schull WJ: Prenatal exposure to atomic radiation and brain damage. Congenital Abnormali-
ties 1989; 29:309-20.
FAA tite “ 0° A. 364438 In Utero Exposure/Cancer Incidence
49.
50.
Delongchamp RR, Mabuchi K, et al.: Cancer mortality among atomic bomb survivors exposed in utero or as young
children, October 1950—May 1992. Radiation Research 1997, 147:385-95.
Preston DL, Cullings H, Suyama A, Funamoto S, Nishi N, Soda M, Mabuchi K, Kodama K, Kasagi F, Shore RE:
Solid cancer incidence in atomic bomb survivors exposed in utero or as young children. Journal of National Cancer
Institute 2008; 100:428—36.
Bih#e H+Hh= Genetic Effects/Birth Defects
JI:
32.
33.
54.
Neel JV, Schull WJ, eds. The Children of Atomic-bomb Survivors: A Genetic Study. Washington DC: National Acad-
emy Press; 1991.
Nakamura N: Genetic effects of radiation in atomic-bomb survivors and their children: Past, present and future. Jour-
nal of Radiation Research (Tokyo) 2006; 47(Suppl):B67-73.
Otake M, Schull WJ, Neel JV: Congenital malformations, stillbirths, and early mortality among children of atomic
bomb survivors: A reanalysis. Radiation Research 1990; 122:1-11.
Hay BE: JECRR BUR DIRE eA IC BES % aE: AS. BUTE, AK. BUN RA WETZE 1999; 34:153-69.
References FSX ff
ihe ttle Genetic Effects/Sex Ratio
55. Schull WJ, Neel JV, Hashizume A: Some further observations on the sex ratio among infants born to survivors of the
atomic bombings of Hiroshima and Nagasaki. American Journal of Human Genetics 1966; 18:328-38.
BiBhxzs 4H Genetic Effects/Chromosome Aberrations
56. BEER : BURA OF UIT TS Sete Hea AES RR RR Ia I HEE LES hh ERR O AA
ROE 1992, OIE ; 1992, pp 307-14.
57. Neel JV, Schull WJ, et al.: The children of parents exposed to atomic bombs: Estimates of the genetic doubling dose
of radiation for humans. Journal of Radiation Research (Tokyo) 1991; 32(Suppl):347-—74. (A review of 45 years’ study
of Hiroshima and Nagasaki atomic-bomb survivors)
iF MRSA RORRE= Genetic Effects/Blood Protein Mutations
58. HERR ATL : ER BU OSE OA ES AAS. CN Re IR EPR TITER ES th. UU O JAK
HOE 1992, MIE ; 1992, pp 323-30.
59. Neel JV, Satoh C, et al.: Search for mutations altering protein charge and/or function in children of atomic-bomb
survivors: Final report. American Journal of Human Genetics 1988; 42:663-76.
60. Neel JV, Satoh C, et al.: The rate with which spontaneous mutation alters the electrophoretic mobility of polypeptides.
Proceedings of the National Academy of Sciences (USA) 1986; 83:389-93.
ie (nh DNA #1 Genetic Effects/DNA Studies
61. Kodaira M, Izumi S, et al.: No evidence of radiation effect on mutation rate at hypervariable minisatellite loci in the
germ cells of atomic-bomb survivors. Radiation Research 2004; 162:350-6.
62. Asakawa J, Nakamura N, et al.: Estimation of mutation induction rates in AT-rich sequences using a genome scanning
approach after X irradiation of mouse spermatogonia. Radiation Research 2007; 168:158—67.
63. Kodaira M, Satoh C, et al.: Lack of effects of atomic-bomb radiation on genetic instability of tandem-repetitive ele-
ments in human germ cells. American Journal of Human Genetics 1995; 57:1275-83.
64. Satoh C, Kodaira M: Effects of radiation on children. Nature 1996; 383:226 (Scientific correspondence).
65. Takahashi N, TsuyamaN, Sasaki K, KodairaM , Satoh Y, KodamaY , Sugita K, K atayama H: Segmental copy-number
variation observed in J apanese by array-CGH. Annals of Human Genetics 2008; 72:193--204.
wiBheS / SCHZEbLUPAHE* Genetic Effects/Mortality and Cancer Incidence
66. Izumi S, Suyama A, et al.: Radiation-related mortality among offspring of atomic bomb survivors: A half-century of
follow-up. International Journal of Cancer 2003; 107:292-7.
67. Izumi S, Koyama K, et al.: Cancer incidence in children and young adults did not increase relative to parental exposure
to atomic bombs. British Journal of Cancer 2003; 89:1709-13.
68. HAY BRL FIR AEERE ¢ SCENE EUBHI SAIC ALS SAMA OBLIR, BORA WIFE 2004; 39:123-9.
‘ie hse Physical Dose Estimates
(SCHR 11 4 BHR, See also reference 11.)
69. Cullings HM, Fujita S, et al.: Dose estimation for atomic bomb survivor studies: Its evolution and present status. Radia-
tion Research 2006; 166:219—54.
70. Straume T, Rugel G, et al.: Measuring fast neutrons in Hiroshima at distances relevant to atomic-bomb survivors.
Nature 2003; 424:539-42.
71. Straume T, Rugel G, et al.: Addendum, Measuring fast neutrons in Hiroshima at distances relevant to atomic-bomb sur-
vivors. Nature 2004; 430:483.
72. Little MP: A dose of the bomb. Nature 2003; 424:495-6.
73. QUURER] : ARS - RI RR Sse Y AF Ls DS86 M bbiet L & MEK DSO2. WRAL 2002; 45:225-32.
74. Young RW, Kerr GD, eds.: Reassessment of the Atomic Bomb Radiation Dosimetry for Hiroshima and Nagasaki—
Dosimetry System 2002. Hiroshima, Japan: Radiation Effects Research Foundation; 2005.
Wh) S25: References
73:
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Bult
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Young RW, Kerr GD #ff : A 545 L ORI IC BT 4 JAF RR Rt © Fa
2002. JA ES : BURNER EMTSEAT + 2000.
FZ BE Residual Radiation
76.
77.
Hasai H, Shizuma K: Residual radiation. Shigematsu I, Ito C, et al., eds. Effects of A-bomb Radiation on the Human
Body. Chur, Switzerland: Harwood Academic Publishers; 1995, pp 387-96.
SESH, FBED YP: RB TICS RR RR I 0 HE HE Tih rae TARERBUN LO \ (KZ 1992,
SCTE | 1992, pp 348-56.
(i
4 FER SHE Biological Dosimetry
(SCHR 26-30, 32, 33 4 BHR. See also references 26-30, 32, and 33.)
78.
79.
80.
81.
82.
83.
Jacob P, Bailiff IK, et al.: Retrospective assessment of exposure to ionizing radiation. International Commission on
Radiation Units and Measurements (ICRU) Report 68. Nuclear Technology Publishing; 2002.
Ay Hh: BL AVR EAR ELA Cy SUBIC L SRB OP. BAR YA LY
A 2007; 9:106-13.
Nakamura N, Miyazawa C, et al.: A close correlation between electron spin resonance (ESR) dosimetry from tooth
4
enamel and cytogenetic dosimetry from lymphocytes of Hiroshima atomic-bomb survivors. International Journal of
Radiation Biology 1998; 73:619-27.
PRILECAY + BOER IS 48 T Z PRAISE PAE FR I Id BT TU a IR EL aah TO SE HE TES ho SUERTE
DMMERZEE 1992, SOE 5 1992, pp 244-52.
Akiyama M: Somatic cell mutations. Shigematsu I, Ito C, et al., eds. Effects of A-bomb Radiation on the Human
Body. Chur, Switzerland: Harwood Academic Publishers; 1995, pp 276-85.
Ishioka N, Umeki S, et al.: Stimulated rapid expression in vitro for early detection of in vivo T-cell receptor mutations
induced by radiation exposure. Mutation Research 1997; 390:269-82.
Sl 1 ReelC ESSEC HR Question 1. How many people died as a result of the atomic
bombings?
84. JA kati Felliy THR Ea oR Ze Si EG + BUNT ORR. HORE: BE + 1979.
85. Committee for the Compilation of Materials on Damage Caused by the Atomic Bombs in Hiroshima and Nagasaki, ed.
Ishikawa E, Swain DL, translators: Hiroshima and Nagasaki. The Physical, Medical, and Social Effects of the Atomic
Bombings. Hiroshima and Nagasaki Cities; 1981.
86. Ohkita T: Annex 4. Health effects on individuals and health services of the Hiroshima and Nagasaki bombs. Effects of
Nuclear War on Health and Health Services and Public Health to Implement Resolution WHA 34.38. Geneva,
Switzerland: World Health Organization; 1984, pp 101-5.
87. Oughterson AW, Warren S: Medical Effects of the Atomic Bomb in Japan. New York: McGraw-Hill; 1956. (This
book was based on the six-volume report of the Joint Commission for the Investigation of the Effects of the Atomic
Bomb in Japan, a team comprising US military and civilian scientists and assembled within a few weeks of the atomic
bombings to work in the field. Copies of the original report are archived at the US National Academy of Sciences,
Washington DC, and in the RERF Hiroshima Library.)
88. RFR al AC PT eB Sith: PRE AC Se OMB LOSS Tit A ASR ATR
& + 1953.
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Radiation Effects Research Foundation
7732-0815 A. Tmax thaw AB 5-2
5-2 Hijiyama Park, Minami-ku, Hiroshima 732-0815 Japan
Tel 082-261-3131 ({t32)
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